The renin-angiotensin system is a far more complex enzymatic cascade than realized previously. Mounting evidence suggests sex-specific differences in the regulation of the renin-angiotensin system and arterial pressure. We examined the hemodynamic responses, angiotensin II receptor subtypes, and angiotensin-converting enzyme 2 gene expression levels after graded doses of angiotensin II in males...

Currently, there is a persisting dispute regarding the renin-angiotensin-aldosterone-system (RAAS) inhibitors' safety of use in COVID-19 pandemics. On one side, RAAS inhibitors appear to determine an overexpression ACE2, receptor SARS-CoV-2. Therefore, they could increase risk SARS-CoV-2 infection and its degree severity. other discontinuation leads cardiovascular decompensation has been discou...

Angiotensin II exerts a mitogenic effect in several in vitro models, but a direct effect on erythroid progenitors has not been documented. Angiotensin-converting enzyme inhibitors and losartan, an angiotensin II type 1 receptor (AT1) antagonist, ameliorate posttransplant erythrocytosis, without altering serum erythropoietin levels. We studied erythroid differentiation and the effect of angioten...

Multiple data suggest that the renin-angiotensin system contributes to the pathogenesis of atherosclerosis. The atherogenic effect of the renin-angiotensin system can only in part be explained by the influence of its effector angiotensin II on blood pressure, smooth muscle cell (SMC) growth, or antifibrinolytic activity. Because chronic inflammation of the vessel wall is a hallmark of atheroscl...

INTRODUCTION: The renin angiotensin system (RAS) is classically known as circulating endocrine system, regulating blood pressure and electrolyte homeostasis. The main effector peptide in this system is Angiotensin II (Ang II), which is hydrolized from angiotensin I (Ang I) by the angiotensin converting enzyme (ACE), a key molecule in this system. Angiotensin I, however, is cleaved from angioten...

It is suggested that vasoconstriction mediated by angiotensin II cleaved from angiotensin I by angiotensin converting enzyme (ACE) is counterbalanced by concomitant formation of vasodilator angiotensin (1-7) by neutral endopeptidase (NEP). Here, we tested this hypothesis using as a bioassay the isolated rat lung perfused with Krebs-Henseleit (KH) solution and ventilated with negative pressures....

Increased glomerular permeability to proteins is a characteristic feature of diabetic nephropathy (DN). The slit diaphragm is the major restriction site to protein filtration, and the loss of nephrin, a key component of the slit diaphragm, has been demonstrated in both human and experimental DN. Both systemic and glomerular hypertension are believed to be important in the pathogenesis of DN. Hu...

Angiotensin II (Ang II) is the most dominant effector component of renin-angiotensin system (RAS) that generally acts through binding to two main classes G protein–coupled receptors, namely Ang subtype 1 receptor (AT1R) and angiotensin 2 (AT2R). Despite some controversial reports, activation AT2R antagonizes effects on AT1R. Studying signaling, function, its specific ligands in cell culture or ...

Angiotensin II (Ang II) is a multi-functional hormone that plays a major role in regulating blood pressure and cardiovascular homoeostasis. The actions of Ang II are mediated by at least two receptor subtypes, designated AT(1) and AT(2). In addition, other angiotensin receptors have been identified which may recognize other angiotensin peptide fragments; however, until now only the AT(1) and AT...