scholarly journals Polar Residues in the Transmembrane Domains of the Type 1 Angiotensin II Receptor Are Required for Binding and Coupling

1996 ◽  
Vol 271 (3) ◽  
pp. 1507-1513 ◽  
Author(s):  
Catherine Monnot ◽  
Claire Bihoreau ◽  
Sophie Conchon ◽  
Kathleen M. Curnow ◽  
Pierre Corvol ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Transmembrane Domains ◽  
Angiotensin Ii Receptor ◽  
Polar Residues

A Review of Angiotensin Receptor Blocker-based Therapies at all Levels of Cardiovascular Risk

2011 ◽  
Vol 7 (4) ◽  
pp. 254 ◽  
Author(s):  
Giuliano Tocci ◽  
Lorenzo Castello ◽  
Massimo Volpe ◽  
◽  
◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Ventricular Hypertrophy ◽  
Renin Angiotensin System ◽  
Left Ventricular ◽  
Clinical Settings ◽  
Angiotensin Ii Receptor ◽  
Angiotensin System ◽  
Receptor Blockers ◽  
Artery Disease

The renin–angiotensin system (RAS) has a key role in the maintenance of cardiovascular homeostasis, and water and electrolyte metabolism in healthy subjects, as well as in several diseases including hypertension, left ventricular hypertrophy and dysfunction, coronary artery disease, renal disease and congestive heart failure. These conditions are all characterised by abnormal production and activity of angiotensin II, which represents the final effector of the RAS. Over the last few decades, accumulating evidence has demonstrated that antihypertensive therapy based on angiotensin II receptor blockers (ARBs) has a major role in the selective antagonism of the main pathological activities of angiotensin II. Significant efforts have been made to demonstrate that blocking the angiotensin II receptor type 1 (AT1) subtype receptors through ARB-based therapy results in proven benefits in different clinical settings. In this review, we discuss the main benefits of antihypertensive strategies based on ARBs in terms of their efficacy, safety and tolerability.

Regulation of Type 1 Angiotensin II Receptor in Adrenal Gland

Hypertension ◽  
1997 ◽  
Vol 30 (3) ◽  
pp. 345-350 ◽  
Author(s):  
Donna H. Wang ◽  
Jingxin Qiu ◽  
Zhaoyong Hu ◽  
Yong Du
Keyword(s):  
Angiotensin Ii ◽  
Adrenal Gland ◽  
Angiotensin Ii Receptor

scholarly journals Functional tests to guide management in an adult with loss of function of type-1 angiotensin II receptor

2021 ◽  
Author(s):  
Daan H. H. M. Viering ◽  
Anneke P. Bech ◽  
Jeroen H. F. de Baaij ◽  
Eric J. Steenbergen ◽  
A. H. Jan Danser ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Collecting Duct ◽  
Perinatal Period ◽  
Tubular Dysfunction ◽  
Loss Of Function ◽  
Angiotensin Ii Receptor ◽  
Salt Wasting ◽  
Truncating Mutation ◽  
Urinary Potassium

AbstractBackgroundGenetic loss of function ofAGT(angiotensinogen),REN(renin),ACE(angiotensin-converting enzyme), orAGTR1(type-1 angiotensin II receptor) leads to renal tubular dysgenesis (RTD). This syndrome is almost invariably lethal. Most surviving patients reach stage 5 chronic kidney disease at a young age.MethodsHere, we report a 28-year-old male with a homozygous truncating mutation inAGTR1(p.Arg216*), who survived the perinatal period with a mildly impaired kidney function. In contrast to classic RTD, kidney biopsy showed proximal tubules that were mostly normal. During the subsequent three decades, we observed evidence of both tubular dysfunction (hyperkalemia, metabolic acidosis, salt-wasting and a urinary concentrating defect) and glomerular dysfunction (reduced glomerular filtration rate, currently ~30 mL/min/1.73 m2, accompanied by proteinuria). To investigate the recurrent and severe hyperkalemia, we performed a patient-tailored functional test and showed that high doses of fludrocortisone induced renal potassium excretion by 155%. Furthermore, fludrocortisone lowered renal sodium excretion by 39%, which would have a mitigating effect on salt-wasting. In addition, urinary pH decreased in response to fludrocortisone. Opposite effects on urinary potassium and pH occurred with administration of amiloride, further supporting the notion that a collecting duct is present and able to react to fludrocortisone.ConclusionsThis report provides living proof that even truncating loss-of-function mutations inAGTR1are compatible with life and relatively good GFR and provides evidence for the prescription of fludrocortisone to treat hyperkalemia and salt-wasting in such patients.

Angiotensin II Receptor Type 1 mRNA is Upregulated in Atria of Patients with End-stage Heart Failure

1997 ◽  
Vol 29 (8) ◽  
pp. 2299-2304 ◽  
Author(s):  
Raffi R Kaprielian ◽  
Emmanuel Dupont ◽  
Sassan Hafizi ◽  
Philip A Poole-Wilson ◽  
Asghar Khaghani ◽  
...  
Keyword(s):  
Heart Failure ◽  
Angiotensin Ii ◽  
Receptor Type ◽  
Angiotensin Ii Receptor ◽  
End Stage Heart Failure ◽  
End Stage

Internalisation of the type I angiotensin II receptor (ATI) and angiotensin II function in the rat adrenal zona glomerulosa cell.

1994 ◽  
Vol 141 (2) ◽  
pp. R5-R9 ◽  
Author(s):  
G. P. Vinson ◽  
M. M. Ho. ◽  
J.R. Puddefoot ◽  
R. Teja ◽  
S. Barker
Keyword(s):  
Monoclonal Antibody ◽  
Plasma Membrane ◽  
Angiotensin Ii ◽  
Zona Glomerulosa ◽  
Type I ◽  
Specific Monoclonal Antibody ◽  
Angiotensin Ii Receptor ◽  
Cellular Localisation ◽  
Glomerulosa Cells

ABSTRACT Little is known about the cellular localisation of the angiotensin II (AII) type 1 receptor (ATI) in the rat adrenal glomerulosa cell, but some studies have suggested that receptor internalisation and recycling may occur. Using a specific monoclonal antibody (6313/G2) to the first extracellular domain, we show here that most of the receptor is internalised in the unstimulated cell. When viable glomerulosa cells are incubated with 6313/G2, the receptor is transiently concentrated on the cell surface, and aldosterone output is stimulated. This stimulated output is enhanced by neither threshold nor maximal stimulatory concentrations of All amide, although the antibody does not inhibit All binding to the receptor. Conversely, the stimulatory actions of the antibody and those of ACTH are additive. The data suggest that recycling to the plasma membrane is constitutive, or regulated by unknown factors. Retention of the ATI receptor in the membrane is alone enough to allow sufficient G protein interaction to generate maximal stimulatory events.

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