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Chronic depression symptoms in Blacks activated the renin-angiotensin-aldosterone-system activity with apparent desensitization of renin activity.
findings indicate that AGT adapts unique serpin features for hormone delivery and binds renin through concerted movements in the N-terminal tail and in its main body to modulate angiotensin release.
Mean blood pressure, plasma Ang II level, and myocardium malondialdehyde (MDA) content of angiotensinogen-renin (AGT-REN) double transgenic hypertension (dTH) mice were higher than those in wild-type (WT) mice.
This study reveals that the human renin protein is able to complement the mouse Ren1d(-/-) non-granulated defect and suggests that granulopoiesis requires a structural motif that is conserved between the mouse Ren1d and human renin proteins.
Findings suggest the prorenin binding to (pro)renin receptor involvement of receptor-associated prorenin system (RAPS) in the pathogenesis of idiopathic epiretinal membrane (iERM).
The current study provides evidence for a possible association of renin gene polymorphisms with essential hypertension in a Han population of northern China.
Plasma renin activity is associated with cardiovascular mortality or heart failure readmissions.
In patients with established atherosclerotic disease undergoing carotid endarterectomy, plasma renin and aldosterone concentrations were not associated with atherosclerotic plaque characteristics. Plasma renin concentration was positively associated with the occurrence of major secondary vascular events.
These observations demonstrate that activation of the renin-angiotensin system (RAS) promotes colitis in a blood pressure independent manner. Angiotensin II appears to drive colonic mucosal inflammation by promoting intestinal epithelial cell apoptosis and mucosal TH17 responses in colitis development
The genotypes of REN, AT1R and AT2R were not associated with the development of preeclampsia in South African Black women.
Urinary angiotensinogen and renin excretion are elevated in CKD patients. Both parameters are negatively associated with eGFR and these associations are independent of urinary albumin excretion
Autosomal dominant polycystic kidney disease (ADPKD), uniquely increases urinary angiotensinogen and renin excretion despite their circulating levels being comparable with those in non-ADPKD chronic kidney disease.
Prospective study of consecutive cardiac disease patients referred for cardiac catheterization has revealed distinct cardiac disease condition-associated differences in the frequencies of elevations in plasma renin, plasma aldosterone concentration, and the aldosterone-renin ratio
Renin-angiotensin system transgenic mouse model suggests that renal injury in preeclampsia may be mediated through local VEGF.
Data suggest mild primary aldosteronism (PA), where plasma renin activity is not as suppressed, is susceptible to dietary sodium influences on renin and ARR (aldosterone to renin ratio). Optimal screening for PA should occur under conditions of high dietary sodium intake (rather than condition of low dietary sodium intake as frequently prescribed for patients with hypertension, which may be a symptom of PA).
Allelic frequency of A of SNP 12109G>A was higher in women with preterm birth than in women with normal vaginal delivery and could be considered a risk factor.
This study demonstrates the efficacy of aldosterone/direct renin concentration ratio as a screening test for primary aldosteronism.
The dominant model (CC vs. CT+TT) of rs1894111 polymorphism in the ADRBK1 gene might be associated with low-renin hypertension in Han Chinese.
Data show that the optimum time for beta-adrenoreceptor antagonists (beta-blockers) withdrawal was 2 weeks when using direct renin concentration (DRC) and 3 weeks for plasma renin activity (PRA).
Active renin was not significantly different between hypertensive patients with and without left ventricular hypertrophy.
Demonstrate substantive conservation of renin regulation across vertebrates, and ultrastructural studies of renin cells reveal at least two distinct morphologies of mesonephric perivascular renin-expressing cells.
Notch signaling and the endothelium are essential for developmental renin expression
first identification of renin gene sequences in zebrafish and the confirmation of renin gene expression in association with zebrafish pronephric and opisthonephric kidneys
Renin catalyzes the first step in the activation pathway of angiotensinogen--a cascade that can result in aldosterone release,vasoconstriction, and increase in blood pressure. Renin, an aspartyl protease, cleaves angiotensinogen to form angiotensin I, which is converted to angiotensin II by angiotensin I converting enzyme, an important regulator of blood pressure and electrolyte balance. Transcript variants that encode different protein isoforms and that arise from alternative splicing and the use of alternative promoters have been described, but their full-length nature has not been determined. Mutations in this gene have been shown to cause familial hyperproreninemia.
, renin precursor, renal
, renin 1 structural
, cathepsin E