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1

VIDEBaeK, AAÖE. "Continued Studies of Plasma-Potassium Levels in Leukemia." Acta Medica Scandinavica 144, no. 2 (April 24, 2009): 160–64. http://dx.doi.org/10.1111/j.0954-6820.1952.tb15679.x.

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2

ADROGUÉ, HORACIO J., ELEANOR D. LEDERER, WADI N. SUKI, and GARABED EKNOYAN. "Determinants of Plasma Potassium Levels in Diabetic Ketoacidosis." Medicine 65, no. 3 (May 1986): 163–72. http://dx.doi.org/10.1097/00005792-198605000-00004.

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3

Leventhal, R. I. "Immediate plasma potassium levels in treating diabetic ketoacidosis." Archives of Internal Medicine 147, no. 8 (August 1, 1987): 1501–2. http://dx.doi.org/10.1001/archinte.147.8.1501.

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4

Alonso, K. "Immediate plasma potassium levels in treating diabetic ketoacidosis." Archives of Internal Medicine 148, no. 3 (March 1, 1988): 750. http://dx.doi.org/10.1001/archinte.148.3.750.

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5

Leventhal, Robert I. "Immediate Plasma Potassium Levels in Treating Diabetic Ketoacidosis." Archives of Internal Medicine 147, no. 8 (August 1, 1987): 1501. http://dx.doi.org/10.1001/archinte.1987.00370080139025.

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6

Alonso, Kenneth. "Immediate Plasma Potassium Levels in Treating Diabetic Ketoacidosis." Archives of Internal Medicine 148, no. 3 (March 1, 1988): 750. http://dx.doi.org/10.1001/archinte.1988.00380030256044.

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7

Rossi, Riccardo, Silvia Savastano, Antonio P. Tommaselli, Rossella Valentino, Vittorio Iaccarino, Libuse Tauchmanova, Antonio Luciano, Marianna Gigante, and Gaetano Lombardi. "Percutaneous computed tomography-guided ethanol injection in aldosterone-producing adrenocortical adenoma." European Journal of Endocrinology 132, no. 3 (March 1995): 302–5. http://dx.doi.org/10.1530/eje.0.1320302.

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Rossi R, Savastano S, Tommaselli AP, Valentino R, Iaccarino V, Tauchmanova L, Luciano A, Gigante M, Lombardi G. Percutaneous computed tomography-guided ethanol injection in aldosteroneproducing adrenocortical adenoma. Eur J Endocrinol 1995;132:302–5. ISSN 0804–4643 The feasibility, safety and effectiveness of percutaneous computed tomography-guided ethanol injection (PEI-CT) was investigated in a patient affected by aldosterone-producing adenoma (APA). A 42-year-old male patient with typical features of hyperaldosteronism presented a solitary left adrenal adenoma measuring 2 cm, with a normal contralateral gland, evidenced by both CT scan and adrenal [75Se-19]-nor-cholesterol scintigraphy. After normalization of potassium plasma levels, 4 ml of sterile 95% ethanol with 0.5 ml of 80% iothalamate sodium was injected. The procedure was completed in about 30 min. No severe pain or local complication was noted. Five hours after PEI, a fourfold and a twofold increase in aldosterone and cortisol plasma levels were observed, respectively. After 11 days on a normal sodium and potassium diet, normal potassium plasma levels and reduced aldosterone plasms levels were present, with reappearance of an aldosterone postural response. Plasma renin activity and aldosterone plasma levels normalized I month later, with reappearance also of a plasma renin activity postural response and maintenance of normal potassium plasma levels even on a high sodium and normal potassium diet. The patient has remained hypertensive, although lower antihypertensive drug dosages have been employed. After 17 months, normal biochemical, hormonal and morphological findings were still present. Thus, we suggest PEI-CT as a further alternative approach to surgery in the management of carefully selected patients with APA. Riccardo Rossi, Chair of Endocrinology, "Federico II" University of Naples, via Sergio Pansini 5, 80131 Naples, Italy
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8

Goldman, Joel M. "Immediate Plasma Potassium Levels in Treating Diabetic Ketoacidosis-Reply." Archives of Internal Medicine 148, no. 3 (March 1, 1988): 752. http://dx.doi.org/10.1001/archinte.1988.00380030256045.

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9

Barnes, J. N., P. J. T. Drew, S. S. Furniss, J. M. P. Holly, A. R. Knight, J. D. Skehan, and F. J. Goodwin. "Effect of angiotensin converting-enzyme inhibition on potassium-mediated aldosterone secretion in essential hypertension." Clinical Science 68, no. 6 (June 1, 1985): 625–30. http://dx.doi.org/10.1042/cs0680625.

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1. Eight patients with essential hypertension were challenged with an infusion of 32 mmol of potassium chloride in saline before and after control of their blood pressure by the angiotensin converting-enzyme (ACE) inhibitor enalapril. 2. The potassium infusion was associated with similar increases in plasma aldosterone before and during enalapril treatment, although absolute aldosterone levels were lower after enalapril treatment despite higher plasma potassium levels. 3. The handling of the potassium load was altered by ACE inhibition. The area under the curve of a plot of the increase in plasma potassium above baseline against time was greater during enalapril treatment than during treatment with placebo. 4. These observations contrast with data obtained in the dog and demonstrate that in patients with essential hypertension stimulation of aldosterone secretion by potassium is not abolished by chronic suppression of plasma angiotensin II; and although plasma aldosterone remains at a lower level, the homoeostasis of plasma potassium is only mildly impaired.
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10

Adam, W. R., A. G. Ellis, and B. A. Adams. "Aldosterone is a physiologically significant kaliuretic hormone." American Journal of Physiology-Renal Physiology 252, no. 6 (June 1, 1987): F1048—F1054. http://dx.doi.org/10.1152/ajprenal.1987.252.6.f1048.

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To study the role of aldosterone in the short-term control of potassium excretion, rats were gavaged with a liquid diet containing 10-20% of their daily caloric and potassium intake, with a range of sodium intakes. Levels of (effective) aldosterone at the time of gavage were manipulated by administration of spironolactone, aldosterone, and adrenalectomy. Urinary sodium, potassium, and creatinine excretion were measured in conscious unrestrained rats for 2 h after the food load, and then blood was collected for measurement of plasma potassium, aldosterone, and renin activity. Potassium excretion was dependent on both dietary potassium and a minimum dietary sodium content. Potassium excretion was reduced by spironolactone and adrenalectomy and increased by acute aldosterone treatment in most dietary groups. These results strongly suggest that the ambient levels of aldosterone are important in determining potassium excretion following food ingestion. Plasma aldosterone was higher with the higher potassium and lower sodium content diets. Changes in plasma aldosterone, with variations in dietary potassium or sodium, suggest a role for aldosterone in subsequent potassium excretion.
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11

Tas, Ayca, Emrullah Hayta, Ahmet Karadag, Cemile Zontul, Esma Ozmen, Süleyman Aydin, and Yavuz Silig. "Potassium Ion Channel Protein (KCNH) Levels in Patients with Fibromyalgia Syndrome." Cellular and Molecular Biology 67, no. 5 (February 4, 2022): 451–57. http://dx.doi.org/10.14715/cmb/2021.67.5.57.

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Although there is not yet full clarity of the pathogenesis of fibromyalgia syndrome (FM), central sensitization is considered to be responsible. The purpose of this study was to measure the plasma levels of potassium ion channel proteins (human KCNH2, KCNH6 and KCNH7) in FM patients and healthy control subjects. The study sample includes 76 newly diagnosed FM patients and 79 healthy individuals. Venous blood samples were taken to measure the plasma levels of KCNH2, KCNH6 and KCNH7. Pain severity in FM patients was assessed using a visual analog scale (VAS). Bioinformatics analysis was performed using the STRING v 11 Protein interaction tool. Age, gender and body mass index were seen to be similar in both groups. In comparisons between FM and control groups, KCNH2 plasma levels was found to be significantly lower in the FM group. No significant correlation was found between plasma levels of KCNH2, KCNH6 and KCNH7 protein levels and VAS score of patients with FM. The KCNH2 protein had a high homology score with 9 proteins. The plasma levels of KCNH2 FM patients were found to be lower than those of the healthy control subjects, no difference was determined in respect of the plasma levels of KCNH6 and KCNH7. These results may be of use in guiding future studies on the pathogenesis of FM.
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12

Goldman, Raimonda, Amir Steinberg, Jennifer Carreiro, Georgia Panagopoulos, Marvin Cooper, and Randy L. Levine. "Pseudonormokalemia in Patients with Thrombocytosis." Blood 114, no. 22 (November 20, 2009): 2420. http://dx.doi.org/10.1182/blood.v114.22.2420.2420.

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Abstract Abstract 2420 Poster Board II-397 Introduction: Pseudohyperkalemia represents an artificial elevation in serum potassium concentration. It is well described that patients with thrombocytosis may have elevated serum but normal plasma potassium. The difference between serum and plasma potassium is felt to be due to potassium release from platelets during clotting. We propose that a similar mechanism will lead to “pseudonormokalemia,” where serum potassium appears to be in the normal range (3.5-5.0 MEq/L) despite below-normal levels in the plasma(<3.5 MEq/L). Method: The interim analysis of this study was sent for consideration to ASH Annual Meeting on November 2006 (108: 3964) We now present the final analysis by comparing 69 thrombocytosis patients (platelets>500,000/uL) to 68 control patients (platelets<500,000/uL). Patients were identified from a list of lab results generated by a computer search and serum and plasma potassium and CBC were then drawn simultaneously. Results: There was no statistically significant difference in sex distribution or age between the two groups. The average platelet count was 667,960/uL in the thrombocytosis group (SD 151,1 uL) and 286,790/uL (SD 103,9 uL) in the control group (p value <0.001). In both groups, serum potassium was higher than plasma potassium. The analysis comparing serum potassium levels between the two groups showed that serum potassium was significantly higher in the thrombocytosis group than in the control. In fact, we found a strong positive correlation (spearman's rho=0.61, p<.001) between platelet count and the difference in values in serum potassium minus plasma potassium. As the platelet count increases, so does the difference between the serum and plasma potassium. The thrombocytosis group was noted to have a difference between serum and plasma potassium of .51 MEq/L (SD .30 MEq/L) while the control group had a difference of .21 MEq/L (SD .20 MEq/L) Conclusion: Patients with thrombocytosis and normal serum potassium may actually be hypokalemic as this study demonstrates. Disclosures: No relevant conflicts of interest to declare.
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13

Kovesdy, Csaba P. "Fluctuations in plasma potassium in patients on dialysis." Nephrology Dialysis Transplantation 34, Supplement_3 (December 1, 2019): iii19—iii25. http://dx.doi.org/10.1093/ndt/gfz209.

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Abstract Plasma potassium concentration is maintained in a narrow range to avoid deleterious electrophysiologic consequences of both abnormally low and high levels. This is achieved by redundant physiologic mechanisms, with the kidneys playing a central role in maintaining both short-term plasma potassium stability and long-term total body potassium balance. In patients with end-stage renal disease, the lack of kidney function reduces the body’s ability to maintain normal physiologic potassium balance. Routine thrice-weekly dialysis therapy achieves long-term total body potassium mass balance, but the intermittent nature of dialytic therapy can result in wide fluctuations in plasma potassium concentration and consequently contribute to an increased risk of arrhythmogenicity. Various dialytic and nondialytic interventions can reduce the magnitude of these fluctuations, but the impact of such interventions on clinical outcomes remains unclear.
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14

Mulkerrin, E., F. H. Epstein, and B. A. Clark. "Aldosterone responses to hyperkalemia in healthy elderly humans." Journal of the American Society of Nephrology 6, no. 5 (November 1995): 1459–62. http://dx.doi.org/10.1681/asn.v651459.

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Plasma aldosterone levels are reported to be lower in healthy elderly individuals compared with young individuals, a difference exaggerated by sodium depletion or upright posture. The aim of this study was to determine the aldosterone response to increases in serum potassium with advancing age. In the Clinical Research Center, six healthy young (20 to 35 yr of age) and six healthy elderly (65 to 85 yr of age) subjects underwent evaluation of their aldosterone responses to potassium infusion (0.5 mEq/kg over 45 min). Both young and elderly subjects had similar basal serum potassium levels (4.3 +/- 0.2 versus 4.4 +/- 0.1 mEq/L), similar sodium and potassium excretion amounts and similar increase in serum potassium levels during infusion (to 5.0 +/- 0.2 versus 5.1 +/- 0.1 mEq/L). However, elderly subjects had lower basal levels of plasma aldosterone and a blunted aldosterone response to potassium infusion (P < 0.05, analysis of variance). Advancing age is characterized by relative hypoaldosteronism in the basal state as well as in response to hyperkalemia. This may contribute to an increased susceptibility to hyperkalemia if other potassium regulatory systems fail.
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15

Dwivedi, Shweta, Urvashi Singh Berman, and Dharmveer Sharma. "Mineral levels in Women with Pre-Eclampsia in Third Trimester of Pregnancy." JOURNAL OF CLINICAL AND BIOMEDICAL SCIENCES 06, no. 1 (March 15, 2016): 28–32. http://dx.doi.org/10.58739/jcbs/v06i1.6.

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Background: Preeclampsia, a systemic illness of late pregnancy seen in approximately 6% of prim-igravid women, is an important cause of maternal and fetal morbidity. The levels of calcium and magnesium in pregnancy may implicate in the possible role in pregnancy induced hypertension (PIH). This study as-sessed serum Ca2+, Mg2+, Na+ and K+ levels in women with PIH. Materials and Methods: We evaluated se-rum potassium, sodium, magnesium and calcium levels in 100 normal pregnant women and 100 women with pre-eclampsia. Result: We found elevated serum potassium levels and reduced calcium, sodium and magnesium levels in pregnant mothers with preeclampsia. Conclusion: Lowered plasma or serum magnesi-um concentrations in pre-eclampsia may contribute to the development in hypertension in pregnancy. In addition, a disturbed Calcium homeostasis is observed in pre-eclampsia. Keywords: Pre-eclampsia, PIH, calcium, magnesium, sodium, potassium
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16

Steinberg, Amir S., Raimonda Goldman, Randy L. Levine, Georgia Panagopoulos, and Marvin C. Cooper. "Pseudonormokalemia in Patients with Thrombocytosis." Blood 108, no. 11 (November 16, 2006): 3964. http://dx.doi.org/10.1182/blood.v108.11.3964.3964.

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Abstract Introduction: Pseudohyperkalemia represents an artificial elevation in serum potassium concentration. It is well described that patients with thrombocytosis may have elevated serum but normal plasma potassium. The difference between serum and plasma potassium is felt to be due to potassium release from platelets during clotting. We propose to prove that a similar mechanism will lead to a "pseudonormokalemia," where serum potassium appears to be in the normal range (3.5–5.0 MEq/L) despite below-normal levels in the plasma(&lt;3.5 MEq/L). Method: This is an interim analysis of a prospective, IRB-approved planned comparison of 146 patients. We compared 36 thrombocytosis patients (platelets&gt;500,000/uL) to 36 control patients (platelets&lt;500,000/uL). Patients were identified from a list of lab results generated by a computer search and serum and plasma potassium and CBC were then drawn concomitantly. The two groups were compared using either the t-test or the Mann-Whitney U test depending on the distribution of the variables. A p &lt;.05 was considered a priori to indicate statistical significance. Results: There was no statistically significant difference in sex distribution or age between the two groups. The average platelet count was 643,190/uL in the thrombocytosis group (SD 134,426 uL) and 280,220/uL (SD 106,217 uL) in the control group with a p value &lt;0.001. While the serum potassium was noted to be significantly different between the two groups, the plasma potassium was not (see table). This was reflected in the difference between the serum and plasma potassium in the two groups. The thrombocytosis group was noted to have a difference between serum and plasma potassium of .52 MEq/L (SD .32 MEq/L) while the control group had a difference of .18 MEq/L (SD .23 MEq/L). The thrombocytosis group had 14 cases in which the difference between serum and plasma potassium was over 0.5 MEq/L whereas the control group had none. Conclusion: In this study, patients with thrombocytosis had higher mean serum potassium levels than the control group but similar mean plasma potassium levels. The mean difference between serum and plasma potassium (Delta) exceeded 0.5 MEq/L in the thrombocytosis arm and there was a statistically significant difference in the Delta values between the two groups. The mean platelet volume (MPV) of the thrombocytosis group was smaller than that of the control group. This indicates that the elevation in serum potassium in the thrombocytosis group cannot be attributed to the actual size of the platelets but rather to the number of platelets involved. Patients with thrombocytosis and normal serum potassium may actually be hypokalemic as this study demonstrates. As we continue to evaluate patients, we believe this difference will become more demonstratable. On interim analysis, our study suggests that in patients with thrombocytosis and normal serum potassium, plasma potassium should be considered along with routine labs. Group Comparison Values (N=36) Thrombocytosis Group-Platelets&gt;500,000/uL Control Group-Platelets&lt;500,000/uL p value Age 60.33 yrs 57.53 yrs p =.50 Serum K+ 4.43 MEq/L 4.15 MEq/L &lt;.001 Plasma K+ 3.91 MEq/L 3.97 MEq/L p =.54 Mean Delta between Serum and Plasma K+ .52 MEq/L (SD .32) .18 MEq/L (SD .23) &lt;0.001 Platelet Count 643.19 X103/uL 280.22X103/uL &lt;0.001 MPV 7.27 fl 8.24 fl &lt;0.001 WBC 12.05 mm3 9.98 mm3 p =.16
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17

Mulkerrin, E. C., F. H. Epstein, and B. A. Clarke. "Changes in Plasma Aldosterone Levels During Potassium Infusion in Elderly Humans." Age and Ageing 24, suppl 1 (January 1, 1995): P13. http://dx.doi.org/10.1093/ageing/24.suppl_1.p13-b.

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18

Whyte, Kenneth F., George J. Addis, Robert Whitesmith, and John L. Reid. "Adrenergic control of plasma magnesium in man." Clinical Science 72, no. 1 (January 1, 1987): 135–38. http://dx.doi.org/10.1042/cs0720135.

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1. Regulation of magnesium balance is poorly understood. However, hypomagnesaemia has been reported in patients in clinical situations where circulating catecholamines are raised including myocardial infarction, cardiac surgery and insulin-induced hypoglycaemia stress tests. 2. The effects of l-adrenaline infusions, sufficient to achieve pathophysiological levels of adrenaline, and of therapeutic intravenous infusions of salbutamol, a β2-agonist, on plasma magnesium, plasma potassium, plasma glucose and plasma insulin levels were studied in a placebo-controlled design in eight normal subjects. 3. Plasma magnesium levels fell significantly during the adrenaline infusion and also during the salbutamol infusion, though more slowly. In a 1 h period of observation after cessation of the infusions no recovery of plasma magnesium levels was seen. Significant falls in plasma potassium levels were also observed during both infusions with spontaneous recovery within 30 min after the infusions. 4. No significant changes in plasma insulin levels occurred with either salbutamol or l-adrenaline compared with control. Plasma glucose levels rose significantly during the adrenaline infusion. 5. The study suggests that both l-adrenaline and salbutamol cause shifts in plasma magnesium which are not mediated by insulin. We propose that intracellular shifts of magnesium occur as a result of β-adrenergic stimulation.
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19

Wen, Wen, Zhaofei Wan, Dong Zhou, Juan Zhou, and Zuyi Yuan. "The Amelioration of Insulin Resistance in Salt Loading Subjects by Potassium Supplementation is Associated with a Reduction in Plasma IL-17A Levels." Experimental and Clinical Endocrinology & Diabetes 125, no. 08 (September 2017): 571–76. http://dx.doi.org/10.1055/s-0042-101793.

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Abstract Background High dietary salt intake contributes to the development of autoimmune/inflammatory diseases including metabolic syndrome (MetS) which potassium supplementation can potentially reverse. T helper (Th) 17 cells as well as its production interleukin (IL)-17A are involved in the pathogenesis of MetS. The polarization of Th17 cells and enhanced IL-17A production induced by high salt might increase the risk of autoimmune/inflammatory diseases. Methods 45 normotensive subjects (aged 29 to 65 years) were enrolled from a rural community of Northern China at random. All of the participants were maintained on a low-salt (3 g/day) diet for 7 days, a high-salt (18 g/day) diet for 7 days, and then a high-salt diet with potassium supplementation (4.5 g/day, KCl) for another 7 days. Insulin resistance (IR) was determined based on the homeostasis model assessment index (HOMA-IR). Results Participants exhibited increased plasma insulin level, as well as progressed HOMA-IR, during a high-salt diet intervention, which potassium supplementation reversed. Moreover, after salt loading, the plasma IL-17A concentrations increased significantly (4.2±2.1 pg/mL to 9.7±5.1 pg/mL; P<0.01), whereas dropped considerably when dietary potassium was supplemented (9.7±5.1 pg/mL to 2.0±0.9 pg/mL; P<0.001). Statistically significant correlations were found between changes in HOMA-IR and changes in plasma IL-17A concentrations during the interventions (low- to high-salt: r=0.642, P<0.01; high-salt to potassium supplementation: r=0.703, P<0.01). Based on multivariate regression analysis, plasma IL-17A showed as an independent predictor of IR. Conclusions The amelioration of salt-loading-induced IR by potassium supplementation in participants may be related to the reduction in plasma IL-17A concentration.
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20

Uyehara, Catherine F. T., and Joy Sarkar. "Role of vasopressin in maintenance of potassium homeostasis in severe hemorrhage." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 305, no. 2 (July 15, 2013): R101—R103. http://dx.doi.org/10.1152/ajpregu.00206.2013.

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Uncontrolled elevation in plasma potassium within minutes of rapid blood volume loss is associated with mortality and distinguishes nonsurvivors of severe hemorrhage from survivors. In a pig model of severe hemorrhage, we discovered that along with a sharp increase in plasma potassium coincident with a shut down of urine flow, nonsurvivors also had an insufficient vasopressin response to hemorrhage. In contrast, survivors did have elevated vasopressin levels in response to hemorrhage and maintained plasma potassium within normal limits. While it has been demonstrated for some time that vasopressin can influence secretion of potassium in the distal nephron, the magnitude of this effect and conditions under which this contributes to physiological modulation of potassium excretion has yet to be defined. In this review, we assess the evidence that would suggest that vasopressin plays a key role in modulating potassium excretion and is important in the regulation of potassium homeostasis during hemorrhage.
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Al-Qusairi, Lama, P. Richard Grimm, Ava M. Zapf, and Paul A. Welling. "Rapid development of vasopressin resistance in dietary K+ deficiency." American Journal of Physiology-Renal Physiology 320, no. 5 (May 1, 2021): F748—F760. http://dx.doi.org/10.1152/ajprenal.00655.2020.

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This study shows that aquaporin-2 regulation is disrupted by a small fall in plasma potassium levels and the response is influenced by sexual dimorphism in renal potassium handling. The findings provided new insights into the mechanisms by which water balance is altered in dietary potassium deficiency and support defining the disorder as “potassium-dependent nephrogenic diabetes insipidus.”
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22

Cai, Yongjiu, Richard C. Ewan, and Dean R. Zimmerman. "Effects of dietary protein and potassium contents on plasma urea nitrogen and amino acids in relation to performance of swine." Canadian Journal of Animal Science 76, no. 3 (September 1, 1996): 351–55. http://dx.doi.org/10.4141/cjas96-052.

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Ninty-six 51 kg-pigs were used to determine effects of dietary protein and potassium levels on concentrations of plasma urea nitrogen (PUN) and free amino acids. Pigs were fed four diets containing 13 or 15% of protein and 0 or 0.4% of potassium addition. Gilts took more days to reach an average weight of 110 kg with lower PUN and less backfat than barrows (P < 0.05), but sex did not affect concentrations of plasma free amino acids (P > 0.10). The pigs fed 15% protein diets had higher PUN (P < 0.01) and plasma threonine and isoleucine (P < 0.05), but lower (P < 0.05) plasma lysine, glutamic acid and glycine than pigs fed 13% protein diets. The 0.4% potassium addition resulted in a tendency to increase PUN (P = 0.06) and a decrease in concentrations of plasma alanine, glutamic acid and glycine (P < 0.05). There was an interaction between protein and potassium treatments (P < 0.05) in which plasma lysine concentration decreased with potassium addition to the 13% protein diet but increased with potassium addition to the 15% protein diet. The results indicate that lower PUN concentrations in gilts were associated with improved efficiency of deposition of dietary nitrogen, resulting in improved carcass grade compared with barrows receiving the same dietary treatments. Key words: Plasma urea nitrogen, free amino acids, protein, potassium, pigs
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23

Rong, Pei, Jennifer L. Wilkinson-Berka, and Sandford L. Skinner. "Potassium control of extrarenal renin secretion in transgenic (mRen-2)27 and normal rats." American Journal of Physiology-Endocrinology and Metabolism 277, no. 4 (October 1, 1999): E631—E638. http://dx.doi.org/10.1152/ajpendo.1999.277.4.e631.

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Plasma active renin and prorenin were followed for 12 h after bilateral, unilateral, and sham nephrectomy (BNx, UNx, and SNx) in anesthetized transgenic (mRen-2)27 rats to compare them with Sprague-Dawley and spontaneously hypertensive rats (SDR and SHR). In Ren-2 rats, active renin and prorenin increased with plasma potassium post-BNx and were augmented by potassium infusion. The increase in prorenin but not active renin was abolished by bilateral adrenalectomy (BADRx). However, this did not reduce prorenin below normal, indicating that the high plasma prorenin Ren-2 phenotype is not only of adrenal origin. SNx and UNx also raised plasma active renin and prorenin in Ren-2 rats, with positive correlations to plasma potassium. In SDR and SHR, active renin fell below prorenin post-BNx, and adrenal ablation and potassium loading (in SDR) modified the decreasing active renin profile consistent with low levels of regulated extrarenal secretion. In Ren-2 rats, adrenal but not extra-adrenal prorenin secretion is potassium sensitive and stress related. The unidentified source of active renin in BNx+BADRx Ren-2 rats is also potassium and stress related.
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Hanton, G., A. Yvon, J.-P. Provost, A. Racaud, and M. Doubovetzky. "Quantitative relationship between plasma potassium levels and QT interval in beagle dogs." Laboratory Animals 41, no. 2 (April 2007): 204–17. http://dx.doi.org/10.1258/002367707780378050.

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25

Hall, TL, A. Barnes, JR Miller, DM Bethencourt, and L. Nestor. "Neonatal mortality following transfusion of red cells with high plasma potassium levels." Transfusion 33, no. 7 (July 1993): 606–9. http://dx.doi.org/10.1046/j.1537-2995.1993.33793325059.x.

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26

Corr, L. A., R. M. Grounds, J. L. Beacham, J. G. Whitwam, and M. J. Brown. "Effects of circulating endogenous catecholamines on plasma glucose, potassium and magnesium." Clinical Science 78, no. 2 (February 1, 1990): 185–91. http://dx.doi.org/10.1042/cs0780185.

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1. To examine the metabolic effects of increases in circulating endogenous plasma catecholamines, we measured plasma glucose, potassium and magnesium in 14 patients undergoing elective coronary artery bypass grafting. The patients were randomized into two groups and received either sodium nitroprusside (a direct-acting vasodilator) or trimetaphan camsylate (a ganglion-blocking agent) for routine control of blood pressure during the operation. 2. There were significant differences between the two groups in the levels of all three metabolic variables studied. Plasma glucose levels rose in both groups, but were significantly higher in the sodium nitroprusside group [peak levels 9.14 (sem 0.72)mmol/l compared with 6.71 (0.88) mmol/l, P< 0.001, analysis of variance]. The cardioplegia solution caused a large increase in plasma magnesium in both groups but in the sodium nitroprusside group the level rose higher [to 1.59 (0.12)mmol/l compared with 1.34 (0.06)mmol/l] and fell faster (P < 0.05, analysis of variance). In the group receiving sodium nitroprusside, plasma potassium fell, by a mean of 0.34 mmol/l, as plasma catecholamine levels rose; no such fall was seen in the group receiving trimetaphan camsylate (P < 0.05, analysis of variance). 3. It is concluded that the sympathoadrenal system is important in causing metabolic changes during cardiopulmonary bypass and may be relevant in other conditions such as acute myocardial infarction.
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Rossetti, L., G. Klein-Robbenhaar, G. Giebisch, D. Smith, and R. DeFronzo. "Effect of insulin on renal potassium metabolism." American Journal of Physiology-Renal Physiology 252, no. 1 (January 1, 1987): F60—F64. http://dx.doi.org/10.1152/ajprenal.1987.252.1.f60.

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The effect of insulin on renal potassium excretion was examined by employing the euglycemic insulin clamp technique in combination with renal clearance measurements. While euglycemia was maintained, insulin was infused at rates of 4.8 (n = 7) and 12 (n = 5) mU X kg-1 X min-1. Steady-state plasma insulin levels of 164 +/- 8 and 370 +/- 15 microU/ml were achieved in the low- and high-dose studies, respectively. Base-line plasma potassium concentration declined progressively by a mean of 0.14 +/- 0.09 (P less than 0.05) and 0.40 +/- 0.05 meq/liter (P less than 0.01) during the low- and high-dose insulin infusion protocols. Urinary potassium excretion did not change significantly from base line with either insulin dose. Because the decline in plasma potassium concentration could have masked a stimulatory effect of insulin on UKV, six rats received a 12-mU X kg-1 X min-1 euglycemic insulin clamp in combination with an exogenous potassium infusion to maintain the plasma potassium concentration constant at the basal level (4.03 +/- 0.03 vs. 4.05 +/- 0.05 meq/l). Under these conditions of normokalemia, insulin augmented UKV 2.4-fold, from 0.20 +/- 0.05 to 0.48 +/- 0.04 meq/l (P less than 0.001).
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28

Houston, A. H., and J. D. Gray. "Red cell magnesium in rainbow trout." Canadian Journal of Zoology 66, no. 4 (April 1, 1988): 929–33. http://dx.doi.org/10.1139/z88-137.

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In vivo erythrocytic magnesium concentration was significantly correlated with red cell potassium level and potassium equilibrium potential, but not with specimen weight, plasma magnesium, red cell sodium and chloride, or chloride equilibrium potential. To examine the relationship between magnesium and potassium, potassium levels were manipulated in vitro with catecholamine, furosemide, ouabain, and valinomycin. Over a wide range of normal and supranormal potassium concentrations, a significant correlation between magnesium and potassium levels was evident. However, depletion of potassium following exposure to ouabain and valinomycin led to a shift from the normal high potassium/low sodium relationship to a high sodium/low potassium state with progressive increases in magnesium content. Correlation of magnesium with potassium was lost, and a significant correlation with red cell sodium, but not with sodium equilibrium potential, was evident. Red cell magnesium concentration appears, therefore, to be influenced by the preponderant univalent cellular cation rather than potassium per se.
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29

Melchinskaya, Ye N., N. I. Gromnatsky, and V. I. Vishnevsky. "Finoptin effect on electrolyte metabolism of diabetics with essential hypertension." Problems of Endocrinology 42, no. 2 (April 15, 1996): 13–15. http://dx.doi.org/10.14341/probl12021.

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It is universally acknowledged that some hypotensive agents may have a negative impact on electrolyte metabolism. This study was aimed at investigating the baseline status of electrolyte metabolism in patients with types I and II diabetes and concomitant essential hypertension and at following up the changes in this parameter over the course of verapamil (finoptin) therapy. Fifty-six patients were followed up. Levels of potassium and sodium in the plasma and red cells, total and ionized calcium in the plasma were measured before therapy and after 0.5, 1.5, and 6 months of finoptin therapy. Higher levels of plasma potassium and red cell sodium were revealed in patients with type I diabetes in comparison with those with type II condition. In patients with noninsulin-dependent diabetes potassium concentrations in red cells and ionized calcium in the plasma were higher. Finoptin therapy promoted a decrease of sodium concentration in the red cells in diabetics with both types I and II condition and a reduction of the level of ionized calcium in the plasma of patients with type II diabetes. Changes in the electrolyte metabolism were transitory and do not require special laboratory monitoring.
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30

Suzuki, H., A. Hishida, K. Ohishi, M. Kimura, and N. Honda. "Role of hormonal factors in plasma K alterations in acute respiratory and metabolic alkalosis in dogs." American Journal of Physiology-Renal Physiology 258, no. 2 (February 1, 1990): F305—F310. http://dx.doi.org/10.1152/ajprenal.1990.258.2.f305.

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Studies were performed on previously nephrectomized dogs to examine roles of hormonal factors in plasma potassium alterations in acute alkalosis. Respiratory and metabolic alkalosis were induced by hyperventilation and intravenous NaHCO3 or tris(hydroxymethyl)aminomethane (Tris) infusion, respectively. Respiratory and NaHCO3-induced alkalosis provoked decreases in plasma potassium from the control value of 5.12 +/- 0.68 (SE) to 4.21 +/- 0.55 meq/l (P less than 0.01) and from 4.65 +/- 0.26 to 3.91 +/- 0.16 meq/l (P less than 0.01) within 180 min, respectively. In contrast, Tris-induced alkalosis elicited an increase in plasma potassium from the control value of 4.56 +/- 0.30 to 5.31 +/- 0.30 meq/l (P less than 0.01). Hypokalemia in respiratory alkalosis was associated with a decrease in the plasma norepinephrine concentration from the control level of 377 +/- 104 to 155 +/- 41 pg/ml (P less than 0.05) but not with changes in plasma levels of epinephrine, insulin, glucagon, cortisol, and aldosterone. However, this hypokalemia was not affected by phentolamine. Also, somatostatin did not modify the hypokalemic response. NaHCO3-induced hypokalemia was associated with a decline in the plasma aldosterone and norepinephrine concentrations. The decline in plasma norepinephrine in NaHCO3-induced alkalosis followed the decrease in plasma potassium. In Tris-induced alkalosis, plasma insulin increased but norepinephrine decreased. The findings do not suggest fundamental roles of the hormonal factors in the plasma potassium alterations in bilaterally nephrectomized dogs with acute alkalosis.
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31

Watanabe, K., K. Hasegawa, and O. Suzuki. "A double-suicide autopsy case of potassium poisoning by intravenous administration of potassium aspartate after intake of some psychopharmaceuticals." Human & Experimental Toxicology 30, no. 7 (July 29, 2010): 777–81. http://dx.doi.org/10.1177/0960327110379250.

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We report a curious double-suicide autopsy case of both male and female who died of potassium poisoning by intravenous administration of concentrated potassium aspartate solution. The plasma concentrations of potassium of the male and female subjects were as high as 49.7 and 62.8 mEq/L, respectively. In addition to the high concentrations of potassium, toxic levels of phenobarbital, promethazine and chlorpromazine, and relatively low levels of etizolam and brotizolam were also detected from whole blood and urine specimens of both cadavers. Twenty empty plastic bottles (10-mL capacity) labeled ‘ASPARA® Potassium Injection 10 mEq’ were found at the suicide spot. To our knowledge, this is the first description for suicidal death by potassium aspartate; in all of the previous literature, they used potassium chloride intravenously or per os.
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32

Yang, Yi, Jingjuan Yang, Xiner Yao, Yu Cui, Xiabing Lang, Binbin Wu, Ping Zhang, and Jianghua Chen. "Association between Blood Potassium Level and Recovery of Postoperative Gastrointestinal Motility during Continuous Renal Replacement Therapy in Patient Undergoing Open Abdominal Surgery." BioMed Research International 2019 (July 2, 2019): 1–8. http://dx.doi.org/10.1155/2019/6392751.

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Background. The aim of this study was to identify the blood potassium level beneficial to the postoperative recovery of gastrointestinal motility during continuous renal replacement therapy (CRRT) in patient undergoing open abdominal surgery. Materials and Methods. 538 critically ill patients after open abdominal surgery and receiving CRRT were retrospectively recruited as the study cohort. Demographic and clinical data were recorded along with an evaluation of the postoperative gastrointestinal motility. Results. Correlation analysis was used to assess the correlation coefficient, and then the variables with correlation coefficient value less than 0.5 were included in the binary logistic regression model. Binary logistic regression model indicated that the postoperative blood potassium level was independently associated with the recovery of gastrointestinal motility (OR=0.109, 95% CI= 0.063 to 0.190, p<0.001). Based on the normal range of blood potassium level, we selected the cut-off point of blood potassium level via Weight of Evidence analysis, which was 4.00 mmol/L. Compared with the patients with insufficient blood potassium levels (plasma potassium concentration < 4.00 mmol/L), those with sufficient blood potassium levels (plasma potassium concentration≥ 4.00 mmol/L) conferred an increase in the rate of 4-day postoperative recovery of gastrointestinal motility (OR= 4.425, 95% CI = 2.933 to 6.667, p<0.001). Conclusions. Maintaining the blood potassium concentrations at a relatively high level of the normal blood potassium range during CRRT would be beneficial to postoperative recovery of gastrointestinal motility.
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33

Yeung, Stanley M. H., Ewout J. Hoorn, Joris I. Rotmans, Ron T. Gansevoort, Stephan J. L. Bakker, Liffert Vogt, and Martin H. de Borst. "Urinary Potassium Excretion, Fibroblast Growth Factor 23, and Incident Hypertension in the General Population-Based PREVEND Cohort." Nutrients 13, no. 12 (December 17, 2021): 4532. http://dx.doi.org/10.3390/nu13124532.

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High plasma fibroblast growth factor 23 (FGF23) and low potassium intake have each been associated with incident hypertension. We recently demonstrated that potassium supplementation reduces FGF23 levels in pre-hypertensive individuals. The aim of the current study was to address whether 24-h urinary potassium excretion, reflecting dietary potassium intake, is associated with FGF23, and whether FGF23 mediates the association between urinary potassium excretion and incident hypertension in the general population. At baseline, 4194 community-dwelling individuals without hypertension were included. Mean urinary potassium excretion was 76 (23) mmol/24 h in men, and 64 (20) mmol/24 h in women. Plasma C-terminal FGF23 was 64.5 (54.2–77.8) RU/mL in men, and 70.3 (56.5–89.5) RU/mL in women. Urinary potassium excretion was inversely associated with FGF23, independent of age, sex, urinary sodium excretion, bone and mineral parameters, inflammation, and iron status (St. β −0.02, p < 0.05). The lowest sex-specific urinary potassium excretion tertile (HR 1.18 (95% CI 1.01–1.37)), and the highest sex-specific tertile of FGF23 (HR 1.17 (95% CI 1.01–1.37)) were each associated with incident hypertension, compared with the reference tertile. FGF23 did not mediate the association between urinary potassium excretion and incident hypertension. Increasing potassium intake, and reducing plasma FGF23 could be independent targets to reduce the risk of hypertension in the general population.
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34

Rutledge, J. C., and L. Rabinowitz. "Kaliuretic regulatory factors in the rat." American Journal of Physiology-Renal Physiology 253, no. 6 (December 1, 1987): F1182—F1196. http://dx.doi.org/10.1152/ajprenal.1987.253.6.f1182.

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To evaluate the role of aldosterone, plasma potassium, and sodium and urine excretion rates in controlling both total daily potassium excretion and the diurnal cyclic excretion of potassium, we performed experiments on unanesthetized, undisturbed rats kept in a 12-h light/12-h dark environment and fed a liquid diet. Independent variations were imposed on potassium intake, sodium intake, and, in groups of adrenalectomized rats, on aldosterone infusion rates. Potassium intake was 2.6, 10.6, and 18.7 meq/day. Sodium intake was 2.1, 6.7, and 17 meq/day. Aldosterone infusion was 0.1, 0.4, 1, and 10 times a basal rate of 1 microgram.day-1.100 g-1, with constant dexamethasone infusion at 1.43 micrograms.day-1.100 g-1. Twenty-four-hour excretion of potassium and sodium balanced 24-h intake of potassium and sodium regardless of the imposed combination of known regulatory factors. The amplitudes of potassium and sodium excretion during the diurnal cycle were each closely related to the ongoing levels of potassium and sodium intake. Plasma potassium was measured at the peak of the potassium cycle. It is suggested, based on analysis of the results, that when caloric balance was maintained, the amplitude of the diurnal potassium cycle was not importantly influenced by the rates of sodium and urine excretion, and, in addition to effects of aldosterone and plasma potassium concentration, the amplitude was importantly influenced by unspecified, homeostatically effective kaliuretic factors. Adrenalectomized rats receiving subbasal aldosterone replacement rejected the high potassium diet, were anuric, lost weight, and were severely hyperkalemic, observations indicating the necessity of adequate aldosterone for maintenance of potassium homeostasis.
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35

I. Ugbor, Chima, Lilian O. Okonkwo, Benson E. Omijie, Nneka J. Duhu, Solomon N. Ekoh, Augusta N. Idenyi, Charles I. Ezema, and Uchechukwu Anthonia E. "Effect of Tobacco Snuff Consumption on Plasma Sodium and Potassium Levels in Rats." Journal of Medical Sciences 22, no. 2 (February 15, 2022): 61–65. http://dx.doi.org/10.3923/jms.2022.61.65.

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36

Noto, Federico, Sandra Recuero, Julián Valencia, Beatrice Saporito, Domenico Robbe, Sergi Bonet, Augusto Carluccio, and Marc Yeste. "Inhibition of Potassium Channels Affects the Ability of Pig Spermatozoa to Elicit Capacitation and Trigger the Acrosome Exocytosis Induced by Progesterone." International Journal of Molecular Sciences 22, no. 4 (February 17, 2021): 1992. http://dx.doi.org/10.3390/ijms22041992.

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During capacitation, sperm undergo a myriad of changes, including remodeling of plasma membrane, modification of sperm motility and kinematic parameters, membrane hyperpolarization, increase in intracellular calcium levels, and tyrosine phosphorylation of certain sperm proteins. While potassium channels have been reported to be crucial for capacitation of mouse and human sperm, their role in pigs has not been investigated. With this purpose, sperm samples from 15 boars were incubated in capacitation medium for 300 min with quinine, a general blocker of potassium channels (including voltage-gated potassium channels, calcium-activated potassium channels, and tandem pore domain potassium channels), and paxilline (PAX), a specific inhibitor of calcium-activated potassium channels. In all samples, acrosome exocytosis was induced after 240 min of incubation with progesterone. Plasma membrane and acrosome integrity, membrane lipid disorder, intracellular calcium levels, mitochondrial membrane potential, and total and progressive sperm motility were evaluated after 0, 120, and 240 min of incubation, and after 5, 30, and 60 min of progesterone addition. Although blocking potassium channels with quinine and PAX prevented sperm to elicit in vitro capacitation by impairing motility and mitochondrial function, as well as reducing intracellular calcium levels, the extent of that inhibition was larger with quinine than with PAX. Therefore, while our data support that calcium-activated potassium channels are essential for sperm capacitation in pigs, they also suggest that other potassium channels, such as the voltage-gated, tandem pore domain, and mitochondrial ATP-regulated ones, are involved in that process. Thus, further research is needed to elucidate the specific functions of these channels and the mechanisms underlying its regulation during sperm capacitation.
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37

Turnamian, S. G., and H. J. Binder. "Electrolyte transport in distal colon of sodium-depleted rats: effect of sodium repletion." American Journal of Physiology-Gastrointestinal and Liver Physiology 255, no. 3 (September 1, 1988): G329—G338. http://dx.doi.org/10.1152/ajpgi.1988.255.3.g329.

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Dietary sodium depletion increases plasma aldosterone level and, as a result, induces amiloride-sensitive electrogenic sodium absorption and electrogenic potassium secretion and stimulates Na+-K+-ATPase activity in rat distal colon, while inhibiting electroneutral sodium chloride absorption. To assess the events that occur as the aldosterone-stimulated colon reverts to normal, unidirectional 22Na and 36Cl fluxes were measured under voltage-clamp conditions across isolated distal colonic mucosa of rats that were initially dietary sodium depleted for 7 days and then sodium repleted for varying periods of time before the study. Within 8 h of dietary sodium repletion, plasma aldosterone level and Na+-K+-ATPase activity declined to normal, amiloride-sensitive electrogenic sodium absorption decreased by greater than 90%, and active electrogenic potassium secretion also decreased markedly. In contrast, electroneutral sodium chloride absorption did not completely return to levels seen in normal animals until approximately 64-88 h. These results demonstrate that maintenance of electrogenic sodium absorption and potassium secretion are directly dependent on elevated plasma aldosterone levels. The inhibition of electroneutral sodium absorption, although initiated by excess aldosterone, persists after normalization of the plasma aldosterone level, thereby implying that the inhibition is dependent on additional factor(s).
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38

Labat, Carlos, Silke Thul, John Pirault, Mohamed Temmar, Simon N. Thornton, Athanase Benetos, and Magnus Bäck. "Differential Associations for Salivary Sodium, Potassium, Calcium, and Phosphate Levels with Carotid Intima Media Thickness, Heart Rate, and Arterial Stiffness." Disease Markers 2018 (December 16, 2018): 1–12. http://dx.doi.org/10.1155/2018/3152146.

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Salivary biomarkers may offer a noninvasive and easy sampling alternative in cardiovascular risk evaluation. The aim of the present study was to establish associations of salivary potassium, sodium, calcium, and phosphate levels with the cardiovascular phenotype determined by carotid ultrasound and carotid-femoral pulse wave velocity and to identify possible covariates for these associations. N=241 samples of nonstimulated whole buccal saliva were obtained from subjects with (n=143; 59%) or without (n=98; 41%) hypertension. The potassium concentrations were 10-fold higher in saliva compared with plasma, whereas sodium concentrations exhibited the reverse relation between saliva and blood. There were no significant correlations between the levels of sodium, potassium, or calcium in saliva and plasma. All salivary electrolytes, except sodium, were significantly associated with age. In age-adjusted analyses, salivary potassium was significantly associated with carotid artery intima media thickness (cIMT) and carotid-femoral pulse wave velocity, and these associations were at the limit of significance in multivariate analyses including prevalent cardiovascular disease and risk factors. Body mass index was a significant confounder for salivary potassium. Salivary phosphate was significantly associated with cIMT in the multivariate analysis. Salivary potassium, calcium, and phosphate levels were significantly associated with heart rate in the univariate age-adjusted as well as in two different multivariate models, whereas no significant associations between sodium and heart rate were observed. In conclusion, the differential association of salivary electrolytes with cardiovascular phenotypes indicates that these electrolytes should be further studied for their predictive value as noninvasive biomarkers for cardiovascular risk evaluation.
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39

Braam, B., P. Boer, and H. A. Koomans. "Tubuloglomerular feedback and tubular reabsorption during acute potassium loading in rats." American Journal of Physiology-Renal Physiology 267, no. 2 (August 1, 1994): F223—F230. http://dx.doi.org/10.1152/ajprenal.1994.267.2.f223.

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Acute hyperkalemia has been associated with changes in reabsorption, glomerular filtration rate (GFR), and autoregulation, which might represent altered tubuloglomerular feedback (TGF) responsiveness. Therefore, TGF responsiveness, segmental reabsorption of water, sodium and potassium, and single-nephron GFR were evaluated during acute potassium loading in male Sprague-Dawley rats. Rats receiving 300 mM KNO3, KHCO3, and KCl showed significantly increased plasma potassium levels and attenuation of stop-flow pressure responses 45-90 min after starting the potassium infusion compared with that observed in time controls and rats infused with 300 mM NaCl. Attenuation of TGF responsiveness could not be related to plasma and kidney angiotensin II levels. Segmental water and sodium handling and proximal to distal single-nephron GFR differences assessed in a time control group and a group receiving 300 mM KCl revealed no changes related to KCl infusion. However, late proximal and early distal potassium concentrations increased significantly from 4.7 +/- 0.2 to 6.3 +/- 0.3 mM (P < 0.01) and from 1.5 +/- 0.1 to 2.7 +/- 0.4 mM (P < 0.01), respectively. In summary, although attenuated TGF responsiveness was demonstrated at higher perfusion rates, this study does not support a significant role for either the TGF mechanism or changes in reabsorption upstream of the early distal tubule for the initiation of kaliuresis during acute potassium loading.
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40

Niri, Tetsuro, Ichiro Horie, Takao Ando, Hiromi Kawahara, Mayu Ueda, Mami Eto, Ayaka Sako, et al. "RENAL FUNCTION AND PLASMA RENIN ACTIVITY AS POTENTIAL FACTORS CAUSING HYPERKALEMIA IN PATIENTS WITH THYROID CARCINOMA UNDERGOING THYROID HORMONE WITHDRAWAL FOR RADIOACTIVE IODINE THERAPY." Endocrine Practice 26, no. 2 (February 2020): 197–206. http://dx.doi.org/10.4158/ep-2019-0374.

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Objective: Hypothyroidism is not commonly considered a cause of hyperkalemia. We previously reported that hyperkalemia was observed mainly in elderly patients treated with renin-angiotensin-aldosterone system (RAS) inhibitors when levothyroxine treatment was withdrawn for the thyroidectomized patients with thyroid carcinoma to undergo radioactive iodine treatment. Here, we investigated whether acute hypothyroidism causes hyperkalemia in patients who were not treated with RAS inhibitors. We also investigated factors influencing potassium metabolism in hypothyroid patients. Methods: We conducted a single-center, prospective cohort study of 46 Japanese patients with thyroid carcinoma undergoing levothyroxine withdrawal prior to radioiodine therapy. All patients were normokalemic before levothyroxine withdrawal. Blood samples were analyzed 3 times: before, and at 3 and 4 weeks after levothyroxine withdrawal. We investigated factors that may be associated with the elevation of serum potassium levels from a euthyroid state to a hypothyroid state. Results: None of the patients developed symptomatic hyperkalemia. The mean serum potassium level was significantly higher at 4 weeks after levothyroxine withdrawal compared to baseline. The serum sodium levels, the estimated glomerular filtration rate (eGFR), and the plasma renin activity (PRA) decreased significantly as hypothyroidism advanced. In contrast, the plasma levels of adrenocorticotropic hormone, cortisol, aldosterone, and antidiuretic hormone were not changed, while serum thyroid hormone decreased. At 4 weeks after their levothyroxine withdrawal, the patients' serum potassium values were significantly correlated with the eGFR and the PRA. Conclusion: Acute hypothyroidism can cause a significant increase in the serum potassium level, which may be associated with a decreased eGFR and decreased circulating RAS. Abbreviations: ACTH = adrenocorticotropic hormone; ADH = antidiuretic hormone; ATPase = adenosine triphosphatase; eGFR = estimated glomerular filtration rate; HbA1c = glycated hemoglobin; K+ = potassium; Na+ = sodium; PRA = plasma renin activity; RAS = renin-angiotensin-aldosterone system; T4 = thyroxine; TSH = thyroid-stimulating hormone
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41

Clareza Arief Wardhana, Anak Agung Wiradewi Lestari, I Nyoman Wande, Sianny Herawati, and Ni Nyoman Mahartini. "Correlation between hemolysis index and storage period to potassium levels of Packed Red Cell in Sanglah General Hospital, Bali, Indonesia." Bali Medical Journal 11, no. 2 (May 20, 2022): 501–5. http://dx.doi.org/10.15562/bmj.v11i2.3604.

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Background: The quality of a blood product is determined by collecting, processing, storing, and transporting it. When blood is stored, there will be mechanical and biochemical changes. Mechanical changes consist of morphological changes and hemolysis, while one of the biochemical changes is increased plasma potassium levels. This study aimed to determine the correlation between the hemolysis index and the storage period to potassium levels of the packed red cell (PRC). Methods: This study was a cross-sectional study at Sanglah Hospital. The sample was taken from the tube in the PRC blood bag and then a complete blood count and potassium analysis were performed. Data were analyzed using SPSS version 25 for Windows. Results: From 70 subjects, the median hemolysis index was 0.15% (0-1.69%), the mean storage period was 12.06±4.95 days, and the mean potassium level was 12.06±3.92 mmol/L. The Spearman test results showed a positive weak significant correlation between the hemolysis index and potassium levels (r=0.360; p=0.002). The Pearson test results also showed a positive weak significant correlation between the parameter of the storage period and potassium levels (r=0.357; p=0.002). Conclusion: There was a positive weak significant correlation between the hemolysis index and the storage period to potassium levels of the PRC.
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42

Tejada, Francisco, Asunción Cremades, Manuel Avilés, Maria T. Castells, and Rafael Peñafiel. "Hypokalemia alters sex hormone and gonadotropin levels: evidence that FSH may be required for luteinization." American Journal of Physiology-Endocrinology and Metabolism 275, no. 6 (December 1, 1998): E1037—E1045. http://dx.doi.org/10.1152/ajpendo.1998.275.6.e1037.

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Hypokalemia produced different effects on steroid sex hormone concentrations in plasma and ovary in the mouse. Estradiol levels were slightly increased, whereas circulating progesterone was markedly decreased in all estrous periods. The preovulatory surge of gonadotropins and the secondary surge of follicle-stimulating hormone (FSH) at estrus were also decreased, but basal levels of both gonadotropins were unaffected. Supplementation with luteinizing hormone (LH), FSH, or gonadotropin-releasing hormone (GnRH) at proestrus rapidly normalized plasma and ovarian progesterone levels at this stage of the estrous cycle. Plasma progesterone levels at diestrus were restored only by combined treatment, at the periovulatory stage, with LH and FSH or GnRH but not by LH or FSH alone. The results demonstrate a lack of steroidogenic activity in the corpus luteum of the potassium-deficient mice and, furthermore, that FSH plays an important role in luteinization in the hypokalemic mice. We conclude that alteration of the transcellular potassium gradient may affect the regulation of the periovulatory surge of gonadotropins and progesterone secretion, probably by altering the release of GnRH from the hypothalamus. In addition, the results suggest that FSH may play a certain role as a luteotropic hormone in mice.
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43

Young, D. B., H. Lin, and R. D. McCabe. "Potassium's cardiovascular protective mechanisms." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 268, no. 4 (April 1, 1995): R825—R837. http://dx.doi.org/10.1152/ajpregu.1995.268.4.r825.

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High rates of potassium intake are associated with protection from cardiovascular diseases in populations consuming primitive diets and in vegetarians living in industrialized cultures. In studies in humans and in animals, a strong inverse association between potassium intake and hypertension and stroke has been described. However, acceptance of the putative protective effect has been limited by inadequate understanding of 1) long-term potassium regulation, and 2) mechanisms by which small changes in plasma potassium concentration may affect development of cardiovascular diseases. In this review, we present results from analyses of long-term potassium regulation that indicated 1) changes in potassium intake may result in potassium concentrations from 3.1 to 4.6 mmol/l, and 2) when the initial rate is below normal, potassium concentration is very sensitive to changes in potassium intake rate. In addition, we present results that provide bases for possible mechanisms by which potassium may protect against cardiovascular diseases: 1) increases in potassium inhibit free radical formation from vascular endothelial cells and macrophages; 2) elevation of potassium inhibits proliferation of vascular smooth muscle cells; 3) platelet aggregation and arterial thrombosis are inhibited by elevation of potassium; and 4) renal vascular resistance is reduced and glomerular filtration rate is increased by elevation of plasma potassium. We propose that elevation of dietary potassium intake increases plasma potassium concentration, thereby inhibiting free radical formation, smooth muscle proliferation, and thrombus formation. As a result, the rate of atherosclerotic lesion formation and thrombosis will be diminished. In addition, we propose the increase in glomerular filtration rate will cause a shift in the relationship between arterial pressure and sodium excretion that will lead to a reduction in arterial blood pressure. By these actions, high levels of dietary intake of potassium could provide the observed protection against the cardiovascular diseases that have plagued humankind since we began eating a modern high-sodium, low-potassium diet.
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44

Lohmeier, Thomas E., Glenn A. Reinhart, H. Leland Mizelle, Maohao Han, and Mark M. Dean. "Renal denervation supersensitivity revisited." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 275, no. 4 (October 1, 1998): R1239—R1246. http://dx.doi.org/10.1152/ajpregu.1998.275.4.r1239.

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To determine whether the chronically denervated kidney is supersensitive to either physiological or pathophysiological plasma levels of norepinephrine (NE), studies were conducted in conscious dogs subjected to unilateral renal denervation and surgical division of the urinary bladder into hemibladders to allow separate 24-h urine collection from denervated and innervated kidneys. Plasma NE concentration was increased by chronic infusion of NE (4–5 days) at rates of 25, 100, and 200 ng ⋅ kg−1 ⋅ min−1. Twenty-four-hour control values for mean arterial pressure (MAP), plasma NE concentration, and ratios for urinary sodium and potassium excretion from denervated and innervated kidneys (Den/Inn) were 94 ± 4 mmHg, 145 ± 24 pg/ml, 1.05 ± 0.05, and 0.97 ± 0.07, respectively. With infusions of NE producing plasma levels of NE of up to ∼3,000 pg/ml or plasma concentrations of NE at least threefold greater than present under most pathophysiological conditions and during acute activation of the sympathetic nervous system, there were no significant long-term changes in MAP or relative excretion rates of sodium and potassium from denervated and innervated kidneys. In marked contrast, pharmacological plasma levels of NE (∼7,000 pg/ml) produced chronic increases in MAP (to 116 ± 2% of control) and sustained reductions in Den/Inn for urinary sodium and potassium excretion to 57 ± 4 and 68 ± 5% of control, respectively, indicating a lower excretion rate of these electrolytes from denervated vs. innervated kidneys. We conclude that the chronically denervated kidney does not exhibit an exaggerated antinatriuretic response to either physiological or pathophysiological levels of circulating NE. It is therefore unlikely that renal denervation supersensitivity is a confounding issue in studies employing chronic renal denervation to elucidate the role of the renal nerves in the regulation of sodium excretion.
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45

Łabno-Kirszniok, Katarzyna, Agata Kujawa-Szewieczek, Andrzej Wiecek, and Grzegorz Piecha. "The Effects of Short-Term Changes in Sodium Intake on Plasma Marinobufagenin Levels in Patients with Primary Salt-Sensitive and Salt-Insensitive Hypertension." Nutrients 13, no. 5 (April 29, 2021): 1502. http://dx.doi.org/10.3390/nu13051502.

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Increased marinobufagenin (MBG) synthesis has been suggested in response to high dietary salt intake. The aim of this study was to determine the effects of short-term changes in sodium intake on plasma MBG levels in patients with primary salt-sensitive and salt-insensitive hypertension. In total, 51 patients with primary hypertension were evaluated during acute sodium restriction and sodium loading. Plasma or serum concentrations of MBG, natriuretic pro-peptides, aldosterone, sodium, potassium, as well as hematocrit (Hct) value, plasma renin activity (PRA) and urinary sodium and potassium excretion were measured. Ambulatory blood pressure monitoring (ABPM) and echocardiography were performed at baseline. In salt-sensitive patients with primary hypertension plasma MBG correlated positively with diastolic blood pressure (ABPM) and serum NT-proANP concentration at baseline and with serum NT-proANP concentration after dietary sodium restriction. In this subgroup plasma MBG concentration decreased during sodium restriction, and a parallel increase of PRA was observed. Acute salt loading further decreased plasma MBG concentration in salt-sensitive subjects in contrast to salt insensitive patients. No correlation was found between plasma MBG concentration and left ventricular mass index. In conclusion, in salt-sensitive hypertensive patients plasma MBG concentration correlates with 24-h diastolic blood pressure and dietary sodium restriction reduces plasma MBG levels. Decreased MBG secretion in response to acute salt loading may play an important role in the pathogenesis of salt sensitivity.
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46

Adil, Ban H., A. S. Obaid, Maysaa R. Naeemah, Diana N. Hashem, and Sala S. Hamza. "Effect of Cold Plasma on the Levels Mineral Blood Components In Vivo." Key Engineering Materials 886 (May 2021): 177–82. http://dx.doi.org/10.4028/www.scientific.net/kem.886.177.

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This study illustrates effect of cold plasma CAP on the mineral blood components in vivo. the mineral blood component (Ca, Na, Cl, K and Fe) are used. Floating Electrode-Dielectric Barrier Discharge (FE-DBD) system of probe diameter 4cm is used for this purpose, and variable voltage (0-20) kV and variable frequency (0-30) kHz, the output power was ranged from (10 - 70) W. the effect of cold atmospheric plasma on mineral blood is studied with different exposure durations (30,45,60) sec. As the plasma exposure duration increases, the calcium, potassium and iron components in the blood increased, while The sodium and chlorine elements decreased. These results give an indication of the cold plasma receptor to be used to treat many diseases related to mineral blood components.
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47

Umakoshi, Hironobu, Ryuichi Sakamoto, Yayoi Matsuda, Maki Yokomoto-Umakoshi, Hiromi Nagata, Tazuru Fukumoto, Masatoshi Ogata, and Yoshihiro Ogawa. "Role of Aldosterone and Potassium Levels in Sparing Confirmatory Tests in Primary Aldosteronism." Journal of Clinical Endocrinology & Metabolism 105, no. 4 (October 29, 2019): 1284–89. http://dx.doi.org/10.1210/clinem/dgz148.

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Abstract Context The current clinical guidelines suggest that confirmatory tests for primary aldosteronism (PA) may be excluded in some of patients who have elevated plasma aldosterone concentration (PAC) under plasma renin suppression. However, this has low-priority evidence and is under debate in use of serum potassium. Objective This study aimed to investigate an appropriate setting for sparing confirmatory tests in PA. Design and Setting A retrospective cross-sectional study in a single referral center. Participants This study included 327 patients who had hypertension under plasma renin suppression and underwent the captopril challenge test (CCT) between January 2007 and April 2019. CCT results were used to diagnose PA. Main Outcome Measure Diagnostic value of PAC and serum potassium in confirmation of PA. Results Of the studied patients, 252 of 327 (77%) were diagnosed with PA. All 61 patients with PAC &gt; 30 ng/dL were diagnosed with PA. In patients with PAC between 20 and 30 ng/dL, 44 of 55 (80%) were diagnosed with PA, while all 26 with PAC between 20 to 30 ng/dL who had spontaneous hypokalemia were diagnosed with PA. The proportion of unilateral PA determined by adrenal vein sampling (AVS) was higher in patients who had PAC &gt; 30 ng/dL or those with spontaneous hypokalemia who had PAC between 20 and 30 ng/dL than those who did not meet the criteria (76% vs. 17%, P &lt; .001). Conclusion Confirmatory tests in PA could be spared in patients who have typical features of PA and these patients had a high probability of unilateral PA on AVS.
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48

Sutjianto, Angeline, Asvin Nurulita, and Fitriani Mangarengi. "KADAR KALIUM DI PACKED RED CELLS SIMPANAN." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 20, no. 2 (March 22, 2018): 147. http://dx.doi.org/10.24293/ijcpml.v20i2.1083.

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Blood transfusion, is not only transferring the blood cells to the recipient, but also transferring other components such as: glucose,lactate, and potassium. When the blood is stored, many alterations occur in its cmponents, particularly a decrease of adenosine5-triphosphate (ATP) and pH, hemolysis, and an increase of potassium levels as well. One of the transfusion complications that should beavoided is hyperkalemia due to the accumulation of potassium that leaks during the storage. However, hyperkalemia related to transfusiondepends not only on the potassium level in the blood unit, but also on its volume and the rate of its blood administration as well. Theaim of this study was to know the potassium levels in stored Packed Red Cell (PRC). A cohort study was done from May–July 2010. Theresearchers used 48 samples from 16 PRCs derived from 16 donors. The samples were drawn from the of PRC hose’s plasma that had beensealed. The potassium levels were measured on the first day, 10th day, and 20th day of the blood collection. The mean potassium levelon the first day was 3.79 mmol/L, 10th day was 12.22 mmol/L and 20th day was 19.77 mmol/L. Comparison of the potassium levelsbetween the first and 10th day, between first and 20th day, and between 10th and 20th day showed a significant difference (p=0.00). Theincrease of potassium levels in the PRC coincide with the storagetime.
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49

Nomura, Kaoru, Doo Chol Han, Kazuko Jibiki, Hiroshi Demura, Toshio Tsushima, and Kazuo Shizume. "Primary aldosteronism with normal aldosterone levels in blood and urine." Acta Endocrinologica 110, no. 4 (December 1985): 522–25. http://dx.doi.org/10.1530/acta.0.1100522.

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Abstract. A 47 year old woman examined for hypertension (200/100 mmHg) was normokalaemic, and had low plasma renin activity (PRA) (0.1 ng/ml · h) and normal aldosterone levels in both plasma (7–13 ng/dl) and urine (4.7–7.4 μg/day). Computed tomography (CT) and scintiscan indicated an adenoma on the right adrenal gland, which was then removed. The histology of the adenoma and analysis of the aldosterone content were compatible with the criteria for an aldosterone-producing adenoma. Three months after surgery, her hypertension had improved, serum potassium levels had increased slightly, and PRA had normalized. This was an unusual form of primary aldosteronism which showed normal levels of aldosterone in both blood and urine.
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50

Uchida, K., S. Azukizawa, N. Imaizumi, T. Kigoshi, I. Yamamoto, H. Hosojima, and S. Morimoto. "Effect of angiotensin II on aldosterone and its precursor steroid production in adrenal zona glomerulosa cells from heparin-treated rats." Acta Endocrinologica 111, no. 2 (February 1986): 222–27. http://dx.doi.org/10.1530/acta.0.1110222.

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Abstract. To assess the nature of the heparin-induced aldosterone deficiency, we investigated the stimulatory effect of angiotensin II (All) on aldosterone and its precursor steroids in adrenal zona glomerulosa cells from heparin-treated rats compared with those in the cells from vehicle-treated rats. Heparin-treated rats had low plasma aldosterone levels, high plasma renin activity and plasma All levels, and normal plasma corticosterone level 6 weeks after the treatment (1500 IU/kg, twice daily). Basal aldosterone production, when corrected to a uniform number of cells per group, was similar in the cells from heparin- and vehicle-treated rats. The cells from heparin-treated rats had a less sensitive and lower response of aldosterone production to All; an increase by 4 orders of magnitude in the threshold dose for All and a decrease in the maximum All-stimulated level. The maximum All-stimulated levels, but not the basal levels, of pregnenolone, corticosterone and 18-OHB production were low in the cells from heparin-treated rats. ACTH caused a similar stimulatory effect on aldosterone production in the cells from heparin- and vehicle-treated rats. The cells from heparin-treated rats had a less sensitive and lower response of aldosterone production to potassium; an increase by one order of magnitude in the threshold dose for potassium and a decrease in the maximum potassium-stimulated level, presumably because of the glomerulosa hyporesponsivness to AII. These results suggest that our heparin-treated rats have selective impairment of adrenal zona glomerulosa cells,
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