Relevant bibliographies by topics / Dahl salt sensitive rat

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Academic literature on the topic 'Dahl salt sensitive rat'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Dahl salt sensitive rat"

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Liu, Yong, Ravinder J. Singh, Kristie Usa, Brian C. Netzel, and Mingyu Liang. "Renal medullary 11β-hydroxysteroid dehydrogenase type 1 in Dahl salt-sensitive hypertension." Physiological Genomics 36, no. 1 (December 2008): 52–58. http://dx.doi.org/10.1152/physiolgenomics.90283.2008.

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The Dahl salt-sensitive rat is a widely used model of human salt-sensitive forms of hypertension. The kidney plays an important role in the pathogenesis of Dahl salt-sensitive hypertension, but the molecular mechanisms involved remain a subject of intensive investigation. Gene expression profiling studies suggested that 11β-hydroxysteroid dehydrogenase type 1 might be dysregulated in the renal medulla of Dahl salt-sensitive rats. Additional analysis confirmed that renal medullary expression of 11β-hydroxysteroid dehydrogenase type 1 was downregulated by a high-salt diet in SS-13BN rats, a consomic rat strain with reduced blood pressure salt sensitivity, but not in Dahl salt-sensitive rats. 11β-Hydroxysteroid dehydrogenase type 1 is known to convert inactive 11-dehydrocorticosterone to active corticosterone. The urinary corticosterone/11-dehydrocorticosterone ratio as well as urinary excretion of corticosterone was higher in Dahl salt-sensitive rats than in SS-13BN rats. Knockdown of renal medullary 11β-hydroxysteroid dehydrogenase type 1 with small-interfering RNA attenuated the early phase of salt-induced hypertension in Dahl salt-sensitive rats and reduced urinary excretion of corticosterone. Knockdown of 11β-hydroxysteroid dehydrogenase type 1 did not affect blood pressure in SS-13BN rats. Long-term attenuation of salt-induced hypertension was achieved with small hairpin RNA targeting renal medullary 11β-hydroxysteroid dehydrogenase type 1. In summary, we have demonstrated that suppression of 11β-hydroxysteroid dehydrogenase type 1 expression in the renal medulla attenuates salt-induced hypertension in Dahl salt-sensitive rats.
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Hong, Nancy J., Agustin Gonzalez-Vicente, Fara Saez, and Jeffrey L. Garvin. "Mechanisms of decreased tubular flow-induced nitric oxide in Dahl salt-sensitive rat thick ascending limbs." American Journal of Physiology-Renal Physiology 321, no. 3 (September 1, 2021): F369—F377. http://dx.doi.org/10.1152/ajprenal.00124.2021.

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The Dahl rat has been used extensively to study the causes and effects of salt-sensitive hypertension. Our study suggests that more complex processes other than simple scavenging of nitric oxide (NO) by superoxide lead to less NO production in thick ascending limbs of the Dahl salt-sensitive rat. The predominant mechanism involved depends on dietary salt. Impaired flow-induced NO production in thick ascending limbs most likely contributes to the Na+ retention associated with salt-sensitive hypertension.
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Gillis, Ellen E., Jan M. Williams, Michael R. Garrett, Jennifer N. Mooney, and Jennifer M. Sasser. "The Dahl salt-sensitive rat is a spontaneous model of superimposed preeclampsia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 309, no. 1 (July 1, 2015): R62—R70. http://dx.doi.org/10.1152/ajpregu.00377.2014.

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The mechanisms of the pathogenesis of preeclampsia, a leading cause of maternal morbidity and death worldwide, are poorly understood in part due to a lack of spontaneous animal models of the disease. We hypothesized that the Dahl salt-sensitive (S) rat, a genetic model of hypertension and kidney disease, is a spontaneous model of superimposed preeclampsia. The Dahl S was compared with the Sprague-Dawley (SD) rat, a strain with a well-characterized normal pregnancy, and the spontaneously hypertensive rat (SHR), a genetic model of hypertension that does not experience a preeclamptic phenotype despite preexisting hypertension. Mean arterial pressure (MAP, measured via telemetry) was elevated in the Dahl S and SHR before pregnancy, but hypertension was exacerbated during pregnancy only in Dahl S. In contrast, SD and SHR exhibited significant reductions in MAP consistent with normal pregnancy. Dahl S rats exhibited a severe increase in urinary protein excretion, glomerulomegaly, increased placental hypoxia, increased plasma soluble fms-like tyrosine kinase-1 (sFlt-1), and increased placental production of tumor necrosis factor-α (TNF-α). The Dahl S did not exhibit the expected decrease in uterine artery resistance during late pregnancy in contrast to the SD and SHR. Dahl S pups and litter sizes were smaller than in the SD. The Dahl S phenotype is consistent with many of the characteristics observed in human superimposed preeclampsia, and we propose that the Dahl S should be considered further as a spontaneous model to improve our understanding of the pathogenesis of superimposed preeclampsia and to identify and test new therapeutic targets for its treatment.
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Tran, Kenneth, June-Chiew Han, Andrew J. Taberner, Carolyn J. Barrett, Edmund J. Crampin, and Denis S. Loiselle. "Myocardial energetics is not compromised during compensated hypertrophy in the Dahl salt-sensitive rat model of hypertension." American Journal of Physiology-Heart and Circulatory Physiology 311, no. 3 (September 1, 2016): H563—H571. http://dx.doi.org/10.1152/ajpheart.00396.2016.

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Salt-induced hypertension leads to development of left ventricular hypertrophy in the Dahl salt-sensitive (Dahl/SS) rat. Before progression to left ventricular failure, the heart initially undergoes a compensated hypertrophic response. We hypothesized that changes in myocardial energetics may be an early indicator of transition to failure. Dahl/SS rats and their salt-resistant consomic controls (SS-13BN) were placed on either a low- or high-salt diet to generate four cohorts: Dahl-SS rats on a low- (Dahl-LS) or high-salt diet (Dahl-HS), and SS-13BN rats on a low- (SSBN-LS) or high-salt diet (SSBN-HS). We isolated left ventricular trabeculae and characterized their mechanoenergetic performance. Our results show, at most, modest effects of salt-induced compensated hypertrophy on myocardial energetics. We found that the Dahl-HS cohort had a higher work-loop heat of activation (estimated from the intercept of the heat vs. relative afterload relationship generated from work-loop contractions) relative to the SSBN-HS cohort and a higher economy of contraction (inverse of the slope of the heat vs. active stress relation) relative to the Dahl-LS cohort. The maximum extent of shortening and maximum shortening velocity of the Dahl/SS groups were higher than those of the SS-13BN groups. Despite these differences, no significant effect of salt-induced hypertension was observed for either peak work output or peak mechanical efficiency during compensated hypertrophy.
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Kushiro, Toshio, Hirotaka Fujita, Ryohei Hisaki, Takae Asai, Izumi Ichiyama, Yasuyuki Kitahara, Miyuki Koike, et al. "Oxidative Stress in the Dahl Salt-Sensitive Hypertensive Rat." Clinical and Experimental Hypertension 27, no. 1 (January 2005): 9–15. http://dx.doi.org/10.1081/ceh-200044244.

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Husted, R. F., T. Takahashi, and J. B. Stokes. "IMCD cells cultured from Dahl S rats absorb more Na+ than Dahl R rats." American Journal of Physiology-Renal Physiology 271, no. 5 (November 1, 1996): F1029—F1036. http://dx.doi.org/10.1152/ajprenal.1996.271.5.f1029.

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Dahl salt-sensitive (S) rats develop hypertension in response to a high-salt diet, whereas Dahl salt-resistant (R) rats do not. There is good evidence that the Dahl S kidneys have diminished natriuretic capacity. We studied the rate of Na+ transport by primary cultures of the inner medullary collecting duct from these two strains to determine whether there were intrinsic differences. Monolayers obtained from prehypertensive S rats transported Na+ at twice the rate as monolayers from age-matched R rats. Mineralocorticoid and glucocorticoid hormones increased Na+ transport from both strains; the S rat monolayers always displayed higher transport rates than R rat monolayers with the same treatment. The Na+ entry pathway in both S and R rat monolayers was via an Na+ channel. The difference in Na+ transport was not explained by a difference in the metabolism of corticosterone, ATP content, citrate synthase activity, ultrastructural appearance, or rate of maturation. Monolayers from S rats tended to have higher protein and DNA content, but these differences could not account for the difference in Na+ transport. Anion secretion in response to adenosine 3',5'-cyclic monophosphate agonists was similar. These results demonstrate intrinsic differences in renal tubular cells that may play an important role in the pathogenesis of salt-sensitive hypertension.
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Hirawa, N., Y. Uehara, Y. Kawabata, A. Numabe, S. Takada, H. Nagoshi, T. Gomi, T. Ikeda, and M. Omata. "Hachimi-jio-gan Extract Protects the Kidney from Hypertensive Injury in Dahl Salt-sensitive Rat." American Journal of Chinese Medicine 24, no. 03n04 (January 1996): 241–54. http://dx.doi.org/10.1142/s0192415x9600030x.

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We investigated whether the Chinese herbal remedy, Hachimi-jio-gan extract, attenuates the renal injury seen in salt-induced hypertension in Dahl salt-sensitive (Dahl S) rats. Administration of this extract for 5 weeks dose-dependently decreased systolic blood pressure in Dahl S rats fed with a high-salt (2% NaCI) diet. This blood pressure reduction was associated with a decrease in cardiac mass and in thickness of the aortic wall. Urinary excretion of prostaglandin E2 was increased and glomerular filtration rate was improved with this treatment. Glomerulosclerosis and arterial injury in the kidney were morphologically improved. These data suggest that Hachimi-jio-gan extract exhibits an antihypertensive effect, which is associated with partial resolution of renal injury in salt-induced hypertension.
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Bugenhagen, Scott M., Allen W. Cowley, and Daniel A. Beard. "Identifying physiological origins of baroreflex dysfunction in salt-sensitive hypertension in the Dahl SS rat." Physiological Genomics 42, no. 1 (June 2010): 23–41. http://dx.doi.org/10.1152/physiolgenomics.00027.2010.

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Salt-sensitive hypertension is known to be associated with dysfunction of the baroreflex control system in the Dahl salt-sensitive (SS) rat. However, neither the physiological mechanisms nor the genomic regions underlying the baroreflex dysfunction seen in this rat model are definitively known. Here, we have adopted a mathematical modeling approach to investigate the physiological and genetic origins of baroreflex dysfunction in the Dahl SS rat. We have developed a computational model of the overall baroreflex heart rate control system based on known physiological mechanisms to analyze telemetry-based blood pressure and heart rate data from two genetic strains of rat, the SS and consomic SS.13BN, on low- and high-salt diets. With this approach, physiological parameters are estimated, unmeasured physiological variables related to the baroreflex control system are predicted, and differences in these quantities between the two strains of rat on low- and high-salt diets are detected. Specific findings include: a significant selective impairment in sympathetic gain with high-salt diet in SS rats and a protection from this impairment in SS.13BN rats, elevated sympathetic and parasympathetic offsets with high-salt diet in both strains, and an elevated sympathetic tone with high-salt diet in SS but not SS.13BN rats. In conclusion, we have associated several important physiological parameters of the baroreflex control system with chromosome 13 and have begun to identify possible physiological mechanisms underlying baroreflex impairment and hypertension in the Dahl SS rat that may be further explored in future experimental and modeling-based investigation.
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Huang, Pan, Yaqian Huang, Boyang Lv, Heng Zhang, Jia Liu, Guosheng Yang, Yinghong Tao, et al. "Endogenous Taurine Downregulation Is Required for Renal Injury in Salt-Sensitive Hypertensive Rats via CBS/H2S Inhibition." Oxidative Medicine and Cellular Longevity 2021 (August 25, 2021): 1–20. http://dx.doi.org/10.1155/2021/5530907.

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Although taurine is known to exert an antihypertensive effect, it is unclear whether it is involved in the mechanism for hypertension-related target organ injury. To reveal the role of endogenous taurine in renal injury formation during salt-sensitive hypertension and clarify its mechanisms, both salt-sensitive Dahl rats and salt-resistant SS-13BN rats were fed a high-salt diet (8% NaCl) and given 2% taurine for 6 weeks. Rat systolic blood pressure (SBP) was measured by the tail-cuff method and artery catheterization. Kidney ultrastructure was observed under an electron microscope. Taurine content and mRNA and protein levels of taurine synthases, cysteine dioxygenase type 1 (CDO1) and cysteine sulfinic acid decarboxylase (CSAD), were decreased in Dahl rats fed a high-salt diet. However, taurine supplementation and the resulting increase in renal taurine content reduced the increased SBP and improved renal function and structural damage in high-salt diet-fed Dahl rats. In contrast, taurine did not affect SS-13BN SBP and renal function and structure. Taurine intervention increased the renal H2S content and enhanced cystathionine-β-synthase (CBS) expression and activity in Dahl rats fed a high-salt diet. Taurine reduced the renin, angiotensin II, and aldosterone contents and the levels of oxidative stress indices in Dahl rat renal tissues but increased antioxidant capacity, antioxidant enzyme activity, and protein expression. However, taurine failed to achieve this effect in the renal tissue of SS-13BN rats fed a high-salt diet. Pretreatment with the CBS inhibitor HA or renal CBS knockdown inhibited H2S generation and subsequently blocked the effect of taurine on renin, superoxide dismutase 1 (SOD1), and superoxide dismutase 2 (SOD2) levels in high-salt-stimulated Dahl renal slices. In conclusion, the downregulation of endogenous taurine production resulted in a decrease in the renal CBS/H2S pathway. This decrease subsequently promoted renin-angiotensin-aldosterone system (RAAS) activation and oxidative stress in the kidney, ultimately contributing to renal injury in salt-sensitive Dahl rats.
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Boegehold, M. A., L. J. Huffman, and G. A. Hedge. "Peripheral vascular resistance and regional blood flows in hypertensive Dahl rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 261, no. 4 (October 1, 1991): R934—R938. http://dx.doi.org/10.1152/ajpregu.1991.261.4.r934.

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The aim of this study was to determine whether different organs undergo similar increases in vascular resistance with hypertension in the Dahl salt-sensitive rat. Cardiac output and organ blood flows were measured with microspheres in anesthetized salt-sensitive and salt-resistant rats fed a high- (7%) or normal- (0.45%) salt diet for 4 wk. High salt intake produced hypertension only in salt-sensitive rats. Cardiac index for the hypertensive group was not different from that for any other group, whereas peripheral resistance index was elevated in proportion to arterial pressure. There were no differences among groups in the fraction of cardiac output supplying the myocardium, intestine, diaphragm, spinotrapezius muscle, or gracilis muscle. The fraction of cardiac output supplying the kidneys was lower in salt-sensitive rats (13%) than in salt-resistant rats (17%) and, among salt-sensitive rats, lowest in the high-salt group. Therefore all the organs studied contribute to increased total peripheral resistance in the hypertensive Dahl rat, with the renal vasculature undergoing the largest resistance increase. Different muscles undergo similar increases in vascular resistance, despite differences in the microvascular abnormalities accompanying salt-induced hypertension.
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Dissertations / Theses on the topic "Dahl salt sensitive rat"

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Garrett, Michael R. "Genetic dissection of hypertension-related renal disease using the Dahl salt-sensitive rat." Connect to Online Resource-OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1175545256.

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Dissertation (Ph.D.)--University of Toledo, 2006.
"In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Sciences." Title from title page of PDF document. Bibliography: p. 89-95, p. 127-131, p. 184-192, p.198-233.
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Garrett, Michael Richard. "Genetic Dissection of Hypertension Related Renal Disease Using the Dahl Salt-Sensitive Rat." University of Toledo Health Science Campus / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=mco1175545256.

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NAGATA, KOHZO, TOYOAKI MUROHARA, XIAN WU CHENG, SHOGO WATANABE, MASAAKI MIYACHI, MAYUKO OHTAKE, MIWA TAKATSU, et al. "Glucocorticoids Activate Cardiac Mineralocorticoid Receptors in Adrenalectomized Dahl Salt- Sensitive Rats." Nagoya University School of Medicine, 2014. http://hdl.handle.net/2237/19484.

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Zhao, Xigeng. "The renin-angiotensin system, cardiac hypertrophy, and salt-sensitive hypertension in Dahl rats." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape4/PQDD_0018/MQ57170.pdf.

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Gabor, Alexander. "Role of Angiotensin II, Glutamate, Nitric Oxide and an Aldosterone-ouabain Pathway in the PVN in Salt-induced Pressor Responses in Rats." Thèse, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/22900.

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High salt intake contributes to the development of hypertension in salt-sensitive humans and animals and the mechanistic causes are poorly understood. In Dahl salt-sensitive (S) but not salt-resistant (R) rats, high salt diet increases cerebrospinal fluid (CSF) [Na+] and activates an aldosterone-mineralocorticoid receptor-epithelial sodium channel-endogenous ouabain (MR-ENaC-EO) neuromodulatory pathway in the brain that enhances the activity of sympatho-excitatory angiotensinergic and glutamatergic pathways, leading to an increase in sympathetic nerve activity (SNA) and blood pressure (BP). We hypothesize that high salt diet in Dahl S rats enhances Ang II release in the paraventricular nucleus (PVN), causing a decrease in local nitric oxide (NO) action and an increase in local glutamate release thereby elevating SNA, BP and heart rate (HR). The present study evaluated the effects of agonists or blockers of MR, ENaC, EO, nitric oxide synthase (NOS) or glutamate and AT1-receptors on the BP and HR responses to acute infusions of Na+ rich aCSF, intracerebroventricularly (icv), or in the PVN of Dahl S, R or Wistar rats or to high salt diet in Dahl S and R rats. In Wistar rats, aldosterone in the PVN enhanced the BP and HR responses to infusion of Na+ rich aCSF in the PVN, but not in the CSF, and only the enhancement was prevented by blockers of MR, ENaC and EO in the PVN. AT1-receptor blockers in the PVN fully blocked the enhancement by aldosterone and the responses to infusion of Na+ rich aCSF icv, or in the PVN. Na+ rich aCSF in the PVN caused larger increases in BP and HR in Dahl S vs. R rats and the responses to Na+ were fully blocked by an AT1-receptor blocker in the PVN. BP and HR responses to a NOS blocker in the PVN were the same, but L-NAME enhanced Na+ effects more in Dahl R than S rats. High salt diet attenuated increases in BP from L-NAME in the PVN of Dahl S but not R rats. AT1 and glutamate receptor blockers candesartan and kynurenate in the PVN decreased BP in Dahl S but not R rats on high salt diet. At the peak BP response to candesartan, kynurenate in the PVN further decreased BP whereas candesartan did not further decrease BP at the peak BP response to kynurenate. Our findings indicate that both an acute increase in CSF [Na+] and high salt intake in Dahl S rats increases AT1-receptor activation and decreases NO action in the PVN thereby contributing to the pressor responses to Na+ and presumably, to dietary salt-induced hypertension. The increased BP response to AT1-receptor activation in the PVN of Dahl S is mediated by enhanced local glutamate receptor activation. An MR-ENaC-EO pathway in the PVN can be functionally active and further studies need to assess its role in Dahl S rats on high salt intake.
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Jones, Rowdy, Jacqueline C. Potter, Shannon C. Allenn, Conor B. Miles, Rhesa Dykes, Michelle M. Duffourc, and Aaron J. Polichnowski. "Striking differences in uromodulin excretion and expression, salt-sensitive hypertension, and renal injury in Dahl SS vs. BN and SS.BN1 consomic rats." Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/asrf/2018/schedule/123.

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Uromodulin (UMOD) is a protein made exclusively in the thick ascending limb. Clinical studies have demonstrated that rare missense mutations in UMOD result in autosomal dominant tubulointerstitial kidney diseases manifest by tubulointerstitial fibrosis (TIF), tubular cysts and a rapid progression to renal failure. In addition, several genome wide association studies reported that common single nucleotide polymorphisms in the UMOD gene are associated with an increased risk of chronic kidney disease (CKD) and hypertension. Interestingly, Dahl salt-sensitive (SS) rats exhibit many of the same pathologies observed in these clinical populations with alterations in UMOD. The goal of this study was to assess the qualitative and quantitative aspects of UMOD via western blotting, and the extent of SS hypertension and proteinuria in Dahl SS vs. a consomic rat strain in which chromosome 1 of the salt-resistant Brown-Norway (BN) rat, harboring the UMOD gene, has been introgressed into the Dahl SS background (SS.BN1). We hypothesized that differences in UMOD would be apparent in SS vs. SS.BN1 rats maintained on a low salt-diet and that the extent of SS hypertension and proteinuria would be attenuated in SS.BN1 vs SS rats. Western blot of urinary UMOD was performed in 16 week old SS (n=5), SS.BN1 (n=7) and BN (n=6) rats maintained on a low salt (LS) diet. BP (radiotelemetry) and proteinuria were assessed during LS feeding and during three weeks of high salt (HS) feeding in a different group of 8-10 week old SS (n=9) and SS.BN1 (n=8) rats. For western blotting, urine was normalized based on the protein concentration, and the density of the 85 kDa UMOD band in SS and SS.BN1 samples were normalized to the average density observed in BN rats. The UMOD band was 4.5 fold higher (p In summary, these data demonstrate striking qualitative and quantitative differences in UMOD between SS and SS.BN1 rats. The pattern of UMOD expression in SS rats is consistent with that observed in some patient populations of UMOD associated kidney disease. Finally, the evidence that SS.BN1 rats, harboring the UMOD gene from BN rats, exhibit significant protection against SS hypertension and proteinuria is consistent with the notion that an alteration in UMOD function may, in part, be responsible for such pathologies in SS rats.
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Breidenbach, Joshua David. "The Development of a Novel Model for Chronic Renal Allograft Rejection." University of Toledo Health Science Campus / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=mco1533298235487342.

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Gadkari, Tushar V. "Effect of Arginine and Oscillatory Ca2+ on Vascular Response Mediated Via Nitric Oxide Signaling in Normal and Salt Sensitive Hypertensive Rat Mesenteric Arterioles." FIU Digital Commons, 2013. http://digitalcommons.fiu.edu/etd/891.

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Hypertension, a major risk factor in the cardiovascular system, is characterized by an increase in the arterial blood pressure. High dietary sodium is linked to multiple cardiovascular disorders including hypertension. Salt sensitivity, a measure of how the blood pressure responds to salt intake is observed in more than 50% of the hypertension cases. Nitric Oxide (NO), as an endogenous vasodilator serves many important biological roles in the cardiovascular physiology including blood pressure regulation. The physiological concentrations for NO bioactivity are reported to be in 0-500 nM range. Notably, the vascular response to NO is highly regulated within a small concentration spectrum. Hence, much uncertainty surrounds how NO modulates diverse signaling mechanisms to initiate vascular relaxation and alleviate hypertension. Regulating the availability of NO in the vasculature has demonstrated vasoprotective effects. In addition, modulating the NO release by different means has proved to restore endothelial function. In this study we addressed parameters that regulated NO release in the vasculature, in physiology and pathophysiology such as salt sensitive hypertension. We showed that, in the rat mesenteric arterioles, Ca2+ induced rapid relaxation (time constants 20.8 ± 2.2 sec) followed with a much slower constriction after subsequent removal of the stimulus (time constants 104.8 ± 10.0 sec). An interesting observation was that a fourfold increase in the Ca2+ frequency improved the efficacy of arteriolar relaxation by 61.1%. Our results suggested that, Ca2+ frequency-dependent transient release of NO from the endothelium carried encoded information; which could be translated into different steady state vascular tone. Further, Agmatine, a metabolite of L-arginine, as a ligand, was observed to relax the mesenteric arterioles. These relaxations were NO-dependent and occurred via α-2 receptor activity. The observed potency of agmatine (EC50, 138.7 ± 12.1 µM; n=22), was 40 fold higher than L-arginine itself (EC50, 18.3 ± 1.3 mM; n = 5). This suggested us to propose alternative parallel mechanism for L-arginine mediated vascular relaxation via arginine decarboxylase activity. In addition, the biomechanics of rat mesentery is important in regulation of vascular tone. We developed 2D finite element models that described the vascular mechanics of rat mesentery. With an inverse estimation approach, we identified the elasticity parameters characterizing alterations in normotensive and hypertensive Dahl rats. Our efforts were towards guiding current studies that optimized cardiovascular intervention and assisted in the development of new therapeutic strategies. These observations may have significant implications towards alternatives to present methods for NO delivery as a therapeutic target. Our work shall prove to be beneficial in assisting the delivery of NO in the vasculature thus minimizing the cardiovascular risk in handling abnormalities, such as hypertension.
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Dutil, Julie. "Identification of blood pressure genes in the Dahl salt-sensitive hypertension model." Thèse, 2005. http://hdl.handle.net/1866/15570.

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Hao, Jing-Ming. "Differences in the expression of opioid peptides in Dahl salt-resistant and salt-sensitive rats." Thesis, 1993. http://hdl.handle.net/2429/1763.

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The Dahl strain of genetically salt-resistant (R) and salt-sensitive (S) rats affords an opportunity to explore mechanisms for the development of hypertension and the consequences, as well as sensitivity or resistance, of salt-induced hypertension. Because of the evidence that opioid peptides and their receptors can be involved in cardiovascular regulation, the objective of this study was to test the hypothesis that /3-endorphin and enkephalins are involved in the development of hypertension through the determination of their precursors preproopiomelanocortin (POMC) and preproenkephalin (ppENK) messenger RNAs in this animal model. Three week old inbred Dahl R and S rats were maintained on high salt diet (8% NaCI) or low salt diet (0.4%) for six weeks. POMCmRNA and ppenk mRNA were examined from tissues of Dahl R and S rats as determinedly Northern blot analysis using p-actin as an internal standard. POMC mRNA was abundant in the pituitary tissues and was not detectable in other tissues. ppenk mRNA was abundantly present in brain, testis and heart. There was more POMC mRNA in the pituitary tissue of R rats on high salt diet compared with the pituitary of S rats on high salt diet. Differences in POMC mRNA in the pituitary were not observed between R and S on low salt diet. There were no differences of ppENK mRNA in the brain between R and S rats on high salt diet. Increased ppENK mRNA was found in the right and left ventricles of the heart of S rats on low salt diet. The increase in ppENK mRNA in the cardiac ventricles of S rats was exaggerated when they were on high salt diet. To define the role of increased ppENK mRNA in the S rats in the regulation of cardiovascular function, the effects of intravenous administration of proenkephalin-derived bioactive peptides Leu5-enkephalin (LE), Met5-enkephalin (ME), Met5-enkephalin-Arg6-Gly7-Leu5 (MEAGL), andMet5-enkephalin-Ard-Phe7 (MEAP) in Sprague-Dawley rats, and effects of these peptides on isolated intact hearts of Sprague-Dawley rats, were examined. At intravenous doses of 3.6 and 36 nmole, none of the opioid peptides had effects on arterial pressure or heart rate. Intravenous administration of LE, ME, MEAGL or MEAP at a dose of 360 nmole per animal briefly deceased the heart rate. The MEAP, but not LE, ME, or MEAGL, induced a more prolonged increase in arterial pressure at the intravenous dose of 360 nmole. LE,ME, MEAGL or MEAP, at concentration 10-6 M in the perfusion solution, had no direct effect on the developed pressure in the left ventricle of the isolated heart. These data show increased preproenkephalin mRNA in the heart and decreased POMC mRNA in the pituitary of Dahl S compared to Dahl R rats. From these results we speculate that: (1)inefficient pituitary production of POMC and consequently J3-endorphin, which is known to decrease arterial pressure, may contribute to the development of hypertension in the S rats on high salt diet; (2) increased release from the heart of the opioid peptide MEAP, and possibly other enkephalins, may be related to the high blood pressure of S rats on low salt diet; (3) exaggerated release of MEAP and/or other enkephalins may exacerbate the process of hypertension in S rats on high salt diet.
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Book chapters on the topic "Dahl salt sensitive rat"

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Peeler, Thomas C., Kenneth M. Baker, Carolina F. Esmurdoc, and Mitchell I. Chernin. "Angiotensin converting enzyme inhibition in Dahl salt-sensitive rats." In Molecular Mechanisms of Cellular Growth, 45–50. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3886-8_6.

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Ogden, P. H., and G. Cramb. "Na+/K+-ATPase Isoform Expression in Cardiac Muscle from Dahl Salt-Sensitive and Salt-Resistant Rats." In The Sodium Pump, 844–47. Heidelberg: Steinkopff, 1994. http://dx.doi.org/10.1007/978-3-642-72511-1_155.

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Kihara, Yasuki, Moriaki Inoko, and Shigetake Sasayama. "Dahl Salt-Sensitive Rats: Model to Study Transitions from Compensatory Hypertrophy to Left Ventricular Failure." In New Horizons for Failing Heart Syndrome, 105–15. Tokyo: Springer Japan, 1996. http://dx.doi.org/10.1007/978-4-431-66945-6_6.

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4

Canessa, Mitzy, and José R. Romero. "Na+ Modulation of K+ Transport by Na+/K+-Pump in Red Cells of Salt-sensitive and Salt-resistant Dahl Rats." In The Sodium Pump, 807–11. Heidelberg: Steinkopff, 1994. http://dx.doi.org/10.1007/978-3-642-72511-1_146.

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Thimm, F., M. Frey, K. Spitzmüller, W. Hofgärtner, and G. Fleckenstein-Grün. "Arteriolar Spasm and Ischemia in the Ocular Fundus of NaCl-Loaded Salt Sensitive Dahl Rats. Vascular Protection by Long-term Treatment with the Calcium Antagonist Nitrendipine." In Oxygen Transport to Tissue XIV, 793–98. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3428-0_97.

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6

Taber, Douglass F. "The Herzon Synthesis of (−)-Acutumine." In Organic Synthesis. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190646165.003.0085.

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Abstract:
The alkaloid (−)-acutumine 3, isolated from the roots of the Chinese moonseed Sinomenium acutum, improves object and social recognition in the Wistar rat model. With four rings and three adjacent, fully-substituted stereogenic centers, 3 presents a significant synthetic challenge. Seth B. Herzon of Yale University assembled (Angew. Chem. Int. Ed. 2013, 52, 3642) 3 by the intramolecular Sakurai cyclization of 1 to 2. The convergent preparation of 1 required the alkyne 10. The literature construc­tion (Org. Lett. 2005, 7, 5075) by A. B. Smith III of the enone 7 from ribose 4 began with protection to 5. Conversion of the primary alcohol to the iodide followed by reduction delivered the aldehyde 6. Addition of vinyl magnesium bromide followed by exposure to the first- generation Grubbs catalyst gave the cyclopentenol, that was oxidized to 7. Conjugate silylation led to the triflate 8, that was carried via coupling with 9 to 10. In earlier work, Professor Herzon had shown (Angew. Chem. Int. Ed. 2011, 50, 8863) that the prochiral quinone from oxidation of 11 could be added to the diene 12 under enantioselective catalysis, to give 13 in high ee. Reduction of the azide gave the imine, that was quaternized with methyl triflate. Addition of the Li salt of 10 to that sensitive intermediate proceeded with high facial selectivity. With aromatiza­tion blocked, the product from the addition of 10 could be thermolyzed to yield 14. The stannylation of the alkyne proceeded with high regio- and stereoselectivity, to give the alkene 1. Exposure of the allylic silane to tetrabutylammonium fluoride drove the desired cyclization to give 2. Chlorination followed by acetonide removal then completed the preparation of the diol 15. The completion of the synthesis required extensive experimentation. Eventually, a protocol was established to oxidize 15 over several steps to the dienone 16. Selective reduction of the ketone (the other carbonyls are vinylogous esters) proceeded with the desired facial selectivity, to give 17. Selective hydrogenation using a Rh catalyst then delivered (−)-acutumine 3. This is the second total synthesis of (−)-acutumine 3. The first, by Steven L. Castle of Brigham Young University (OHL October 5, 2009), is quite different. It is instruc­tive to compare the two side by side.
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Conference papers on the topic "Dahl salt sensitive rat"

1

Zhao, Dan, Zhipei Huang, and Jiankang Wu. "Multiscale Entropy Analysis of Blood Pressure Variability in Dahl Salt-sensitive Rats." In ICBBB '21: 2021 11th International Conference on Bioscience, Biochemistry and Bioinformatics. New York, NY, USA: ACM, 2021. http://dx.doi.org/10.1145/3448340.3448351.

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2

Westwood, Brian, and Mark Chappell. "Application of correlate summation to data clustering in the estrogen- and salt-sensitive female mRen2.Lewis rat." In the 1st international workshop. New York, New York, USA: ACM Press, 2006. http://dx.doi.org/10.1145/1183535.1183542.

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