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Journal articles on the topic 'Resine angiotensine'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Meng, Q. C., J. Durand, Y. F. Chen, and S. Oparil. "Effects of dietary salt on angiotensin peptides in kidney." Journal of the American Society of Nephrology 6, no. 4 (1995): 1209–15. http://dx.doi.org/10.1681/asn.v641209.

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This study used a novel simple method for the extraction, separation, identification, and quantitation of angiotensin-like immunoactivity from tissue to examine the effects of altering dietary NaCl intake on intrarenal angiotensin I, II, and III levels in salt-sensitive, spontaneously hypertensive rats, salt-resistant Wistar-Kyoto rats, and Sprague-Dawley rats. Seven-week-old male spontaneously hypertensive rats, Wistar-Kyoto rats, and Sprague-Dawley rats were assigned randomly to a diet containing either 8% (high) or 1% (basal) salt and were maintained on these diets for 3 wk. Rats were then

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2

Zangrillo, Alberto, Sergio Colombo, Anna Mara Scandroglio, et al. "Angiotensin II infusion and markers of organ function in invasively ventilated COVID-19 patients." Critical Care and Resuscitation 23, no. 2 (2021): 215–24. http://dx.doi.org/10.51893/2021.2.oa9.

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OBJECTIVE: The use of angiotensin II in invasively ventilated patients with coronavirus disease 2019 (COVID-19) is controversial. Its effect on organ function is unknown. DESIGN: Prospective observational study. SETTING: Intensive care unit (ICU) of a tertiary academic hospital in Milan, Italy. PARTICIPANTS: Adult patients receiving mechanical ventilation due to COVID-19. INTERVENTIONS: Use angiotensin II either as rescue vasopressor agent or as low dose vasopressor support. MAIN OUTCOME MEASURES: Patients treated before angiotensin II was available or treated in an adjacent COVID-19 ICU serve

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3

Selvam, R., K. C. Rohini, C. Arunan, and K. P. Subashchandran. "Synthesis of Biologically Important Angiotensin-II and Angiotensin-IV Peptides by Using 4-(2',4'-Dimethoxypenyl-Fmoc-Aminomethyl)phenoxy Resin." Asian Journal of Chemistry 25, no. 15 (2013): 8673–76. http://dx.doi.org/10.14233/ajchem.2013.14998.

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4

Raff, H., and B. Jankowski. "Inhibition of aldosterone release by hypoxia in vitro: interaction with carbon monoxide." Journal of Applied Physiology 76, no. 2 (1994): 689–93. http://dx.doi.org/10.1152/jappl.1994.76.2.689.

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We have demonstrated that the aldosteronogenic pathway of the zona glomerulosa is unusually sensitive to modest changes in PO2 (Michaelis constant for O2 approximately 95 Torr). The current study evaluated the interaction of CO (the classic ligand for P-450 enzymes) and the decreases in O2 on aldosteronogenesis in vitro. Bovine adrenocortical zona glomerulosa cells were incubated for 2 h and stimulated with either adenosine 3′,5′-cyclic monophosphate (cAMP) or angiotensin II. Ten and 20% CO led to significant decreases in cAMP- and angiotensin II-stimulated aldosteronogenesis. The combination

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5

Edwards, Aurélie, and Thomas L. Pallone. "Mechanisms underlying angiotensin II-induced calcium oscillations." American Journal of Physiology-Renal Physiology 295, no. 2 (2008): F568—F584. http://dx.doi.org/10.1152/ajprenal.00107.2008.

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To gain insight into the mechanisms that underlie angiotensin II (ANG II)-induced cytoplasmic Ca2+ concentration ([Ca]cyt) oscillations in medullary pericytes, we expanded a prior model of ion fluxes. ANG II stimulation was simulated by doubling maximal inositol trisphosphate (IP3) production and imposing a 90% blockade of K+ channels. We investigated two configurations, one in which ryanodine receptors (RyR) and IP3 receptors (IP3R) occupy a common store and a second in which they reside on separate stores. Our results suggest that Ca2+ release from stores and import from the extracellular sp

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6

Leckenby, Simon, and Timothy Chimunda. "Terlipressin rescue therapy in renin-aldosterone-angiotensin system dysregulation induced shock." Australian Critical Care 33 (2020): S35. http://dx.doi.org/10.1016/j.aucc.2020.04.110.

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7

Gur, Yael, Haim Breitbart, Yehudit Lax, Sara Rubinstein, and Nadav Zamir. "Angiotensin II induces acrosomal exocytosis in bovine spermatozoa." American Journal of Physiology-Endocrinology and Metabolism 275, no. 1 (1998): E87—E93. http://dx.doi.org/10.1152/ajpendo.1998.275.1.e87.

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Ejaculated mammalian spermatozoa must reside in the female genital tract for some time before gaining the ability to fertilize the egg. During this time, spermatozoa undergo some physiological changes that collectively are called capacitation. Capacitation of mammalian spermatozoa is a prerequisite for acrosome reaction, which is an exocytotic event occurring before fertilization. The specific biophysical and biochemical changes that accompany sperm capacitation and the agonists inducing acrosome reaction are not fully understood. Using SDS-gel electrophoresis and immunoblotting, we demonstrat

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8

Lee, Shin-Hann, Sarah M. Gomes, Judy Ghalayini, Konstantin G. Iliadi, and Gabrielle L. Boulianne. "Angiotensin Converting Enzyme Inhibitors and Angiotensin Receptor Blockers Rescue Memory Defects in Drosophila-Expressing Alzheimer’s Disease-Related Transgenes Independently of the Canonical Renin Angiotensin System." eneuro 7, no. 6 (2020): ENEURO.0235–20.2020. http://dx.doi.org/10.1523/eneuro.0235-20.2020.

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9

Sun, Bei, Jonathan S. Williams, Luminita Pojoga, et al. "Renin gene polymorphism: its relationship to hypertension, renin levels and vascular responses." Journal of the Renin-Angiotensin-Aldosterone System 12, no. 4 (2011): 564–71. http://dx.doi.org/10.1177/1470320311405873.

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The renin gene has been previously reported to be associated with essential hypertension in a variety of ethnic groups. However, no studies have systematically evaluated the relationship between single nucleotide polymorphisms (SNPs) representing coverage of the entire renin gene and hypertension risk. To evaluate the association between renin gene variation and hypertension we investigated data on HyperPATH cohort with 570 hypertensive and 222 normotensive Caucasian subjects. Six tagging SNPs and resultant haplotypes were tested for associations with hypertension risk, followed by mean arteri

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10

Royea, Jessika, Maria Lacalle-Aurioles, Lianne J. Trigiani, Alice Fermigier, and Edith Hamel. "AT2R’s (Angiotensin II Type 2 Receptor’s) Role in Cognitive and Cerebrovascular Deficits in a Mouse Model of Alzheimer Disease." Hypertension 75, no. 6 (2020): 1464–74. http://dx.doi.org/10.1161/hypertensionaha.119.14431.

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Antihypertensive medications targeting the renin-angiotensin system have lowered the incidence and progression of Alzheimer disease. Understanding how these medications function could lead to novel therapeutic strategies. AT4Rs (angiotensin IV receptors) have been associated with angiotensin receptor blockers’ cognitive, cerebrovascular, and neuroinflammatory rescue in Alzheimer disease models. Yet, whether AT4Rs act alone or with AT2Rs remains unknown. Here, we investigated whether AT2Rs contribute to losartan’s benefits and whether chronic AT2R activation could mimic angiotensin receptor blo

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11

Fitts, D. A. "Angiotensin II receptors in SFO but not in OVLT mediate isoproterenol-induced thirst." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 267, no. 1 (1994): R7—R15. http://dx.doi.org/10.1152/ajpregu.1994.267.1.r7.

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Thirst elicited by the beta-adrenergic agonist isoproterenol in rats depends in part on the secretion of renin, the consequent synthesis of angiotensin II (ANG II), and the binding of circulating ANG II to dipsogenic receptors in the brain. These receptors probably reside in either of two forebrain circumventricular organs, the subfornical organ (SFO) or organum vasculosum laminae terminalis (OVLT). Experiments determined that lesions of the SFO, but not of the OVLT, reduced drinking induced by isoproterenol treatment. Competitive ANG II-receptor antagonism with sarthran reduced isoproterenol-

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12

Yvan-Charvet, Laurent, Florence Massiéra, Noël Lamandé, et al. "Deficiency of Angiotensin Type 2 Receptor Rescues Obesity But Not Hypertension Induced by Overexpression of Angiotensinogen in Adipose Tissue." Endocrinology 150, no. 3 (2008): 1421–28. http://dx.doi.org/10.1210/en.2008-1120.

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Increased angiotensinogen (AGT) production by white adipose tissue has been related to not only obesity but also hypertension. Several studies have highlighted the importance of the angiotensin II type 2 receptor (AT2) in the regulation of blood pressure and fat mass, but the relevance of this transporter in a physiopathological model of increased AGT production, as it occurs in obesity, has not yet been investigated. We used transgenic mice that display either a deletion of AT2 (AT2 KO), an overexpression of AGT (OVEX), or both compound mutants (KOVEX). Results demonstrated that adipocyte hyp

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13

He, Hongli, Ling Liu, Qihong Chen, et al. "Mesenchymal Stem Cells Overexpressing Angiotensin-Converting Enzyme 2 Rescue Lipopolysaccharide-Induced Lung Injury." Cell Transplantation 24, no. 9 (2015): 1699–715. http://dx.doi.org/10.3727/096368914x685087.

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14

Easterling, T. "Low-dose, short-acting, angiotensin-converting enzyme inhibitors as rescue therapy in pregnancy." Obstetrics & Gynecology 96, no. 6 (2000): 956–61. http://dx.doi.org/10.1016/s0029-7844(00)01037-1.

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15

PRYDE, P. "Low-dose, short-acting, angiotensin-converting enzyme inhibitors as rescue therapy in pregnancy." Obstetrics & Gynecology 97, no. 5 (2001): 799. http://dx.doi.org/10.1016/s0029-7844(01)01371-0.

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16

EASTERLING, THOMAS R., DARCY B. CARR, CONNIE DAVIS, CYDNEY DIEDERICHS, DEBRA A. BRATENG, and BARBARA SCHMUCKER. "Low-Dose, Short-Acting, Angiotensin-Converting Enzyme Inhibitors as Rescue Therapy in Pregnancy." Obstetrics & Gynecology 96, no. 6 (2000): 956–61. http://dx.doi.org/10.1097/00006250-200012000-00017.

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17

Pryde, Peter G., and Mason Barr. "LOW-DOSE, SHORT-ACTING,ANGIOTENSIN-CONVERTING ENZYME INHIBITORS AS RESCUE THERAPY IN PREGNANCY." Obstetrics & Gynecology 97, no. 5 (2001): 799. http://dx.doi.org/10.1097/00006250-200105000-00031.

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18

Easterling, Thomas R. "LOW-DOSE, SHORT-ACTING,ANGIOTENSIN-CONVERTING ENZYME INHIBITORS AS RESCUE THERAPY IN PREGNANCY." Obstetrics & Gynecology 97, no. 5 (2001): 799–800. http://dx.doi.org/10.1097/00006250-200105000-00032.

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19

Funk, Steven D., Raymond H. Bayer та Jeffrey H. Miner. "Endothelial cell-specific collagen type IV-α3expression does not rescue Alport syndrome inCol4a3−/−mice". American Journal of Physiology-Renal Physiology 316, № 5 (2019): F830—F837. http://dx.doi.org/10.1152/ajprenal.00556.2018.

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The glomerular basement membrane (GBM) is a critical component of the kidney’s blood filtration barrier. Alport syndrome, a hereditary disease leading to kidney failure, is caused by the loss or dysfunction of the GBM’s major collagen type IV (COL4) isoform α3α4α5. The constituent COL4 α-chains assemble into heterotrimers in the endoplasmic reticulum before secretion into the extracellular space. If any one of the α3-, α4-, or α5-chains is lost due to mutation of one of the genes, then the entire heterotrimer is lost. Patients with Alport syndrome typically have mutations in the X-linked COL4A

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20

Kule, Chris E., Vijaya Karoor, Jonathan N. E. Day та ін. "1029-176 Rescue of internalization-impaired angiotensin II AT1 mutants by β-arrestin overexpression". Journal of the American College of Cardiology 43, № 5 (2004): A455—A456. http://dx.doi.org/10.1016/s0735-1097(04)91923-7.

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21

Santos, Edson L., Rosana I. Reis, Ronaldo G. Silva, et al. "Functional rescue of a defective angiotensin II AT1 receptor mutant by the Mas protooncogene." Regulatory Peptides 141, no. 1-3 (2007): 159–67. http://dx.doi.org/10.1016/j.regpep.2006.12.030.

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22

Robert, Martine, David De Bels, Martin Chaumont, Patrick M. Honoré, and Philippe Gottignies. "Angiotensin converting enzyme inhibitor intoxication: Naloxone to the rescue? Naloxone for ACE inhibitor intoxication." American Journal of Emergency Medicine 37, no. 6 (2019): 1217.e1–1217.e2. http://dx.doi.org/10.1016/j.ajem.2019.03.046.

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23

Poulsen, Knud, Arne Høj Nielsen, and Arne Johannessen. "Measurement of inactive renin in normal, nephrectomized, and adrenalectomized rats." Canadian Journal of Physiology and Pharmacology 69, no. 9 (1991): 1381–84. http://dx.doi.org/10.1139/y91-205.

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In a new method for measurement of inactive rat plasma renin, the trypsin generated angiotensin I immunoreactive material, which was HPLC characterized as similar to tetradecapeptide renin substrate, is removed by a cation exchange resin before the renin incubation step. The method also corrects for trypsin destruction of endogenous angiotensinogen by the addition of exogenous angiotensinogen. When measured with this method inactive renin in rat plasma decreased after nephrectomy and increased after adrenalectomy. This is in accordance with findings in humans. A sexual dimorphism of prorenin (

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24

Bridgeman, Mary Barna, Milisha Shah, and Edward Foote. "Potassium-lowering agents for the treatment of nonemergent hyperkalemia: pharmacology, dosing and comparative efficacy." Nephrology Dialysis Transplantation 34, Supplement_3 (2019): iii45—iii50. http://dx.doi.org/10.1093/ndt/gfz223.

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Abstract Hyperkalemia represents a common and potentially life-threating electrolyte abnormality, a complication frequently observed in patients with heart failure, kidney disease, diabetes or in those receiving drug therapies influencing the renin–angiotensin–aldosterone system. Elevated serum potassium levels are often the result of impaired urinary potassium elimination, inadequate or reduced cellular potassium uptake, severe heart failure, use of medications influencing potassium levels in the circulation, or, more commonly, a combination of these factors. Strategies for the treatment of n

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25

Lakhani, Hari Vishal, Mishghan Zehra, Sneha S. Pillai, et al. "Beneficial Role of HO-1-SIRT1 Axis in Attenuating Angiotensin II-Induced Adipocyte Dysfunction." International Journal of Molecular Sciences 20, no. 13 (2019): 3205. http://dx.doi.org/10.3390/ijms20133205.

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Background: Angiotensin II (Ang II), released by the renin–angiotensin–aldosterone system (RAAS), contributes to the modulatory role of the RAAS in adipose tissue dysfunction. Investigators have shown that inhibition of AngII improved adipose tissue function and insulin resistance in mice with metabolic syndrome. Heme Oxygenase-1 (HO-1), a potent antioxidant, has been demonstrated to improve oxidative stress and adipocyte phenotype. Molecular effects of high oxidative stress include suppression of sirtuin-1 (SIRT1), which is amenable to redox manipulations. The mechanisms involved, however, in

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26

EASTERLING, T. "Low-dose, short-acting, angiotensin-converting enzyme inhibitors as rescue therapy in pregnancy: In reply." Obstetrics & Gynecology 97, no. 5 (2001): 799–800. http://dx.doi.org/10.1016/s0029-7844(01)01391-6.

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27

Manley-Casco, Dario, and Paul Berkowitz. "A Whole Food Plant-Based Diet With a Novel Potassium-Binding Resin in a Patient With Advanced Chronic Kidney Disease." American Journal of Lifestyle Medicine 14, no. 6 (2020): 592–94. http://dx.doi.org/10.1177/1559827620951036.

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Chronic kidney disease (CKD) is a major health problem with substantial morbidity and mortality. Plant-based diets decrease the incidence of CKD and progression of kidney disease and help prevent and treat the important comorbidities of obesity, type 2 diabetes, hypertension, and cardiovascular disease. However, in patients with CKD, there is concern that a plant-based diet may contribute to life-threatening hyperkalemia. We present a patient with CKD secondary to hypertensive glomerulosclerosis that worsened despite standard of care treatment. Shared decision making was used to initiate a who

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28

Sharma, Ravindra K., Aline C. Oliveira, Tao Yang, et al. "Gut Pathology and Its Rescue by ACE2 (Angiotensin-Converting Enzyme 2) in Hypoxia-Induced Pulmonary Hypertension." Hypertension 76, no. 1 (2020): 206–16. http://dx.doi.org/10.1161/hypertensionaha.120.14931.

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Therapeutic advances for pulmonary hypertension (PH) have been incremental because of the focus on the pulmonary vasculature in PH pathology. Here, we evaluate the concept that PH is, rather, a systemic disorder involving interplay among multiorgan systems, including brain, gut, and lungs. Therefore, the objective of this study was to evaluate the hypothesis that PH is associated with a dysfunctional brain-gut-lung axis and that global overexpression of ACE2 (angiotensin-converting enzyme 2) rebalances this axis and protects against PH. ACE2 knockin and wild-type (WT; C57BL/6) mice were subjec

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29

HALLINAN, E. ANN. "Formation of a dehydroalanyl residue from S-benzylcysteine upon HF cleavage of a [Sar1, Cys8]-angiotensin II peptide resin." International Journal of Peptide and Protein Research 38, no. 6 (2009): 601–2. http://dx.doi.org/10.1111/j.1399-3011.1991.tb01546.x.

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30

Langeveld, B. E., R. H. Henning, B. J. G. L. de Smet, et al. "Rescue of arterial function by angiotensin-(1-7): towards improvement of endothelial function by drug-eluting stents." Netherlands Heart Journal 16, no. 9 (2008): 293–98. http://dx.doi.org/10.1007/bf03086167.

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31

Vashistha, Himanshu, Pravin C. Singhal, Ashwani Malhotra, et al. "Null mutations at the p66 and bradykinin 2 receptor loci induce divergent phenotypes in the diabetic kidney." American Journal of Physiology-Renal Physiology 303, no. 12 (2012): F1629—F1640. http://dx.doi.org/10.1152/ajprenal.00246.2012.

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Candidate genes have been identified that confer increased risk for diabetic glomerulosclerosis (DG). Mice heterozygous for the Akita (Ins2+/C96Y) diabetogenic mutation with a second mutation introduced at the bradykinin 2 receptor (B2R−/−) locus express a disease phenotype that approximates human DG. Src homology 2 domain transforming protein 1 (p66) controls mitochondrial metabolism and cellular responses to oxidative stress, aging, and apoptosis. We generated p66-null Akita mice to test whether inactivating mutations at the p66 locus will rescue kidneys of Akita mice from disease-causing mu

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32

Zhang, Fengxiang, Zhang Wang, and Shiying Xu. "Macroporous resin purification of grass carp fish (Ctenopharyngodon idella) scale peptides with in vitro angiotensin-I converting enzyme (ACE) inhibitory ability." Food Chemistry 117, no. 3 (2009): 387–92. http://dx.doi.org/10.1016/j.foodchem.2009.04.015.

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33

Gao, Xiujun, Xiqi Li, Peisheng Yan, Rui Sun, Guangfeng Kan, and Ying Zhou. "Identification and Functional Mechanism of Novel Angiotensin I Converting Enzyme Inhibitory Dipeptides from Xerocomus badius Cultured in Shrimp Processing Waste Medium." BioMed Research International 2018 (2018): 1–9. http://dx.doi.org/10.1155/2018/5089270.

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ACE inhibitory dipeptides from Xerocomus badius fermented shrimp processing waste were isolated with ethanol, macroporous resin, chloroform, and Sephadex G-10 in sequence and identified by LC-MS/MS system coupled with electrospray ionization source. Molecular docking was performed for exploring the mechanism of their inhibitions. The results showed that the identified ACE inhibitory dipeptides were Cys-Cys and Cys-Arg with IC50 values of 4.37 ± 0.07 and 475.95 ± 0.11 μM, respectively. The difference between ACE inhibitor potency of Cys-Cys and Cys-Arg could be explained by results of molecular

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34

Barreto-Chaves, M. L., and M. Mello-Aires. "Effect of luminal angiotensin II and ANP on early and late cortical distal tubule HCO3- reabsorption." American Journal of Physiology-Renal Physiology 271, no. 5 (1996): F977—F984. http://dx.doi.org/10.1152/ajprenal.1996.271.5.f977.

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Bicarbonate reabsorption was evaluated by stationary microperfusion “in vivo“ early distal (ED) and late distal (LD) segments of at kidney. Intratubular pH was recorded by double-barreled of H+ exchange resin/reference (1 M KCl) microelectrodes for the determination of HCO3- reabsorption. In the presence of angiotensin II (ANG II) (10(-12) M), a significant increase in HCO3- reabsorption was observed both in ED (from 0.930 +/- 0.060 to 2.64 +/- 0.210 nmol.cm-2.s-1 in luminally perfused tubules and from 0.850 +/- 0.040 to 2.03 +/- 0.210 nmol.cm-2.s-1 during capillary perfusion) and LD segments

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35

Kanduri, Swetha Rani, Kathryn J. Suchow, and Juan Carlos Q. Velez. "A Rare Case of Patiromer Induced Hypercalcemia." Journal of Clinical Medicine 10, no. 16 (2021): 3756. http://dx.doi.org/10.3390/jcm10163756.

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Patiromer is a calcium (Ca)-potassium (K) exchange resin approved for the treatment of hyperkalemia. Disorders of Ca or acid base balance were not reported in pre-approval clinical trials. We present a case of a patient with chronic kidney disease (CKD) with an unusual picture of hypercalcemia, metabolic alkalosis and hypokalemia upon intensification of patiromer dosing. A 56-year-old white man with CKD stage 4 (baseline creatinine 2.8 mg/dL) due to type 1 diabetes mellitus, proteinuria (1.5 g/g) and persistently high serum potassium 5.9 mEq/L attributed to type 4 renal tubular acidosis was ev

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36

Rubio Campal, José Manuel, Hugo Del Castillo, Belén Arroyo Rivera, et al. "Improvement in quality of life with sacubitril/ /valsartan in cardiac resynchronization non-responders: The RESINA (RESynchronization plus an Inhibitor of Neprilysin/Angiotensin) registry." Cardiology Journal 28, no. 3 (2021): 402–10. http://dx.doi.org/10.5603/cj.a2021.0009.

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Doyle, M. P., and B. R. Walker. "Attentuation of systemic vasoreactivity in chronically hypoxic rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 260, no. 6 (1991): R1114—R1122. http://dx.doi.org/10.1152/ajpregu.1991.260.6.r1114.

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Experiments were performed to assess the effects of chronic hypoxia on systemic vasoreactivity in conscious unrestrained rats and in abdominal aortic rings. Two groups of rats were used: normoxic controls and chronically hypoxic rats that were maintained in a hypobaric chamber (380 mmHg) for 4 wk before experimentation. In conscious animals instrumented with pulsed Doppler cardiac output probes and arterial and venous catheters, mean arterial pressure and mean cardiac output were measured before and during graded continuous infusions of phenylephrine (PE), angiotensin II, and arginine vasopres

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Pawlik, Marek J., Barbara Miziak, Aleksandra Walczak, et al. "Selected Molecular Targets for Antiepileptogenesis." International Journal of Molecular Sciences 22, no. 18 (2021): 9737. http://dx.doi.org/10.3390/ijms22189737.

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The term epileptogenesis defines the usually durable process of converting normal brain into an epileptic one. The resistance of a significant proportion of patients with epilepsy to the available pharmacotherapy prompted the concept of a causative treatment option consisting in stopping or modifying the progress of epileptogenesis. Most antiepileptic drugs possess only a weak or no antiepileptogenic potential at all, but a few of them appear promising in this regard; these include, for example, eslicarbazepine (a sodium and T-type channel blocker), lamotrigine (a sodium channel blocker and gl

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39

Thomas, Walter G., Thomas J. Motel, Christopher E. Kule, Vijay Karoor, and Kenneth M. Baker. "Phosphorylation of the Angiotensin II (AT1A) Receptor Carboxyl Terminus: A Role in Receptor Endocytosis." Molecular Endocrinology 12, no. 10 (1998): 1513–24. http://dx.doi.org/10.1210/mend.12.10.0179.

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Abstract The molecular mechanism of angiotensin II type I receptor (AT1) endocytosis is obscure, although the identification of an important serine/threonine rich region (Thr332Lys333Met334Ser335Thr336Leu337Ser338) within the carboxyl terminus of the AT1A receptor subtype suggests that phosphorylation may be involved. In this study, we examined the phosphorylation and internalization of full-length AT1A receptors and compared this to receptors with truncations and mutations of the carboxyl terminus. Epitope-tagged full-length AT1A receptors, when transiently transfected in Chinese hamster ovar

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40

Li, Xiao C., Gary E. Shull, Elisa Miguel-Qin, Fang Chen, and Jia L. Zhuo. "Role of the Na+ /H+ exchanger 3 in angiotensin II-induced hypertension in NHE3-deficient mice with transgenic rescue of NHE3 in small intestines." Physiological Reports 3, no. 11 (2015): e12605. http://dx.doi.org/10.14814/phy2.12605.

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41

Liu, Peidang, Xiuying Bai, Heming Wang, Andrew Karaplis, David Goltzman, and Dengshun Miao. "Hypophosphatemia-mediated hypotension in transgenic mice overexpressing human FGF-23." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 4 (2009): H1514—H1520. http://dx.doi.org/10.1152/ajpheart.00581.2009.

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Fibroblast growth factor-23 (FGF-23) is a potent circulating phosphaturic factor associated with renal phosphate wasting. The effects of FGF-23 on skeletal and phosphate homeostasis have been investigated widely; however, the effect of FGF-23 on the cardiovascular system (CVS) is unknown. To assess whether FGF-23 influences the function and structure of the CVS and whether the effect of FGF-23 on the CVS is mediated by FGF receptors directly or indirectly by hypophosphatemia, FGF-23 transgenic mice and their wild-type littermates were fed a normal diet or a high-phosphate diet comprising a nor

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Yosri, Nermeen, Aida A. Abd El-Wahed, Reem Ghonaim, et al. "Anti-Viral and Immunomodulatory Properties of Propolis: Chemical Diversity, Pharmacological Properties, Preclinical and Clinical Applications, and In Silico Potential against SARS-CoV-2." Foods 10, no. 8 (2021): 1776. http://dx.doi.org/10.3390/foods10081776.

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Propolis, a resin produced by honeybees, has long been used as a dietary supplement and folk remedy, and more recent preclinical investigations have demonstrated a large spectrum of potential therapeutic bioactivities, including antioxidant, antibacterial, anti-inflammatory, neuroprotective, immunomodulatory, anticancer, and antiviral properties. As an antiviral agent, propolis and various constituents have shown promising preclinical efficacy against adenoviruses, influenza viruses, respiratory tract viruses, herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2), human immunodeficiency virus

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Andrukhova, Olena, Svetlana Slavic, Ute Zeitz, et al. "Vitamin D Is a Regulator of Endothelial Nitric Oxide Synthase and Arterial Stiffness in Mice." Molecular Endocrinology 28, no. 1 (2014): 53–64. http://dx.doi.org/10.1210/me.2013-1252.

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Abstract The vitamin D hormone 1α,25-dihydroxyvitamin D3 [1,25(OH)2D3] is essential for the preservation of serum calcium and phosphate levels but may also be important for the regulation of cardiovascular function. Epidemiological data in humans have shown that vitamin D insufficiency is associated with hypertension, left ventricular hypertrophy, increased arterial stiffness, and endothelial dysfunction in normal subjects and in patients with chronic kidney disease and type 2 diabetes. However, the pathophysiological mechanisms underlying these associations remain largely unexplained. In this

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Qie, Shuyan, Yuanyuan Ran, Xiaosheng Lu та ін. "Candesartan modulates microglia activation and polarization via NF-κB signaling pathway". International Journal of Immunopathology and Pharmacology 34 (січень 2020): 205873842097490. http://dx.doi.org/10.1177/2058738420974900.

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Microglia are diverse cells that acquire different functional phenotypes in response to microenvironment in which they reside. Several transcriptional regulators have been identified that regulate different microglia phenotypes. They are mainly stimulated into two opposing phenotypes, classically (M1) and alternatively (M2) phenotype. Regulating microglia polarization from M1 to M2 state has been suggested as a potential therapeutic approach in treatment of CNS disorders. Candesartan, an angiotensin II type I receptors antagonist, exerts beneficial effects for antioxidant, anti-inflammation, n

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Xiao, Liang, Luciana Simao do Carmo, Jason D. Foss, Wei Chen, and David G. Harrison. "Sympathetic Enhancement of Memory T-Cell Homing and Hypertension Sensitization." Circulation Research 126, no. 6 (2020): 708–21. http://dx.doi.org/10.1161/circresaha.119.314758.

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Rationale: Effector memory T lymphocytes (T EM cells) exacerbate hypertension in response to repeated hypertensive stimuli. These cells reside in the bone marrow for prolonged periods and can be reactivated on reexposure to the hypertensive stimulus. Objective: Because hypertension is associated with increased sympathetic outflow to the bone marrow, we hypothesized that sympathetic nerves regulate accumulation and reactivation of bone marrow–residing hypertension-specific T EM cells. Methods and Results: Using unilateral superior cervical ganglionectomy in wild-type C57BL/6 mice, we showed tha

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Lai, Yanxian, Jianyong Li, Lintao Zhong, et al. "The pseudogene PTENP1 regulates smooth muscle cells as a competing endogenous RNA." Clinical Science 133, no. 13 (2019): 1439–55. http://dx.doi.org/10.1042/cs20190156.

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AbstractThe long non-coding RNA (lncRNA) PTENP1 is a pseudogene of phosphatase and tensin homologue deleted on chromosome ten (PTEN), has been implicated in smooth muscle cell (SMC) proliferation and apoptosis. PTENP1 is the pseudogene of PTEN. However, it is unclear whether and how PTENP1 functions in the proliferation and apoptosis of human aortic SMCs (HASMCs). Here, we hypothesised that PTENP1 inhibits HASMC proliferation and enhances apoptosis by promoting PTEN expression. PCR analysis and Western blot assays respectively showed that both PTENP1 and PTEN were up-regulated in human aortic

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Venketasubramanian, Narayanaswamy, Craig Anderson, Hakan Ay, et al. "Stroke Care during the COVID-19 Pandemic: International Expert Panel Review." Cerebrovascular Diseases 50, no. 3 (2021): 245–61. http://dx.doi.org/10.1159/000514155.

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<b><i>Background:</i></b> Coronavirus disease 2019 (COVID-19) has placed a tremendous strain on healthcare services. This study, prepared by a large international panel of stroke experts, assesses the rapidly growing research and personal experience with COVID-19 stroke and offers recommendations for stroke management in this challenging new setting: modifications needed for prehospital emergency rescue and hyperacute care; inpatient intensive or stroke units; posthospitalization rehabilitation; follow-up including at-risk family and community; and multispecialty depart

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Kwiatkowski, Boguslaw A., ZhaoMing Dong, and Robert E. Richard. "The Identification of Genes Cooperating with Mpl Signaling Using Insertional Mutagenesis." Blood 112, no. 11 (2008): 3860. http://dx.doi.org/10.1182/blood.v112.11.3860.3860.

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Abstract In addition to its role in megakaryopoiesis and platelet production, thrombopoietin activation of its receptor, myeloproliferative leukemia virus protooncogene (Mpl), results in hematopoietic stem cell (HSC) homeostasis and self-renewal. Mutations in the Mpl gene have been shown to be associated with myeloproliferative disorders. In an attempt to identify genes that could cooperate with Mpl signaling leading to an increase in cell survival and proliferation, we have used retroviral expression of a drug dependent, dimerizable, fusion protein which contains the cytoplasmic domain of Mpl

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Olry de Labry Lima, Antonio, Óscar Díaz Castro, Jorge M. Romero-Requena, et al. "Hyperkalaemia management and related costs in chronic kidney disease patients with comorbidities in Spain." Clinical Kidney Journal, April 7, 2021. http://dx.doi.org/10.1093/ckj/sfab076.

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Abstract Background Hyperkalaemia (HK) is a common electrolyte disorder in patients with chronic kidney disease (CKD) and/or treated with renin–angiotensin–aldosterone system inhibitors (RAASis). The aim of this study is to determine the severity, current management and cost of chronic HK. Methods We performed a retrospective cohort study of patients with chronic HK and CKD, heart failure or diabetes mellitus between 2011 and 2018. The study follow-up was 36 months. Results A total of 1499 patients with chronic HK were analysed: 66.2% presented with mild HK, 23.4% with moderate HK and 10.4% wi

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Ismail, Umar, Kiran Sidhu, and Shelley Zieroth. "Hyperkalaemia in Heart Failure." Cardiac Failure Review 7 (May 12, 2021). http://dx.doi.org/10.15420/cfr.2020.29.

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Hyperkalaemia has become an increasingly prevalent finding in patients with heart failure (HF), especially with renin–angiotensin–aldosterone system (RAAS) inhibitors and angiotensin–neprilysin inhibitors being the cornerstone of medical therapy. Patients living with HF often have other comorbidities, such as diabetes and chronic kidney disease, which predispose to hyperkalaemia. Until now, we have not had any reliable or tolerable therapies for the treatment of hyperkalaemia to facilitate implementation or achievement of target doses of RAAS inhibition. Patiromer sorbitex calcium and sodium z

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