Response to Cardiovascular Effects of Nonproteolytic Activation of Prorenin

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Cardiovascular effects of nonproteolytic activation of prorenin.

Cardiovascular Effects of Nonproteolytic Activation of Prorenin To the Editor: Several articles have appeared recently on the role of tissue prorenin in the pathogenesis of cardiovascular and renal damage in experimental models of hypertension and diabetes mellitus1–3 including the study by Ichihara et al,3 published in Hypertension and accompanied by an editorial comment.4 Thus, in rats with s...

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Nonproteolytic activation of prorenin contributes to development of cardiac fibrosis in genetic hypertension.

In contrast to proteolytic activation of inactive prorenin by cleavage of the N-terminal 43 residue peptide, we found that prorenin is activated without proteolysis by binding of the prorenin receptor to the pentameric "handle region" I(11P)LLKK(15P). We hypothesized that such activation occurs in hypertensive rats and causes cardiac renin-angiotensin system (RAS) activation and end-organ damag...

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Suppression of ocular inflammation in endotoxin-induced uveitis by inhibiting nonproteolytic activation of prorenin.

PURPOSE A recent study revealed that angiotensin receptor signaling mediates ocular inflammation and neovascularization. It was also found that prorenin undergoes nonproteolytic activation leading to upregulation of the renin-angiotensin system (RAS) when prorenin receptor interacts specifically with the handle region of prorenin. The purpose of the present study was to elucidate the role of th...

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Receptor-mediated nonproteolytic activation of prorenin and induction of TGF-β1 and PAI-1 expression in renal mesangial cells.

While elevated plasma prorenin levels are commonly found in diabetic patients and correlate with diabetic nephropathy, the pathological role of prorenin, if any, remains unclear. Prorenin binding to the (pro)renin receptor [(p)RR] unmasks prorenin catalytic activity. We asked whether elevated prorenin could be activated at the site of renal mesangial cells (MCs) through receptor binding without...

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Nonproteolytic "activation" of prorenin by active site-directed renin inhibitors as demonstrated by renin-specific monoclonal antibody.

Incubation of human plasma prorenin (PR), the enzymatically inactive precursor of renin (EC 3.4.23.15), with a number of nonpeptide high-affinity active site-directed renin inhibitors induces a conformational change in PR, which was detected by a monoclonal antibody that reacts with active renin but not with native inactive PR. This conformational change also occurred when inactive PR was activ...

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ژورنال

عنوان ژورنال: Hypertension

سال: 2006

ISSN: 0194-911X,1524-4563

DOI: 10.1161/01.hyp.0000247257.33104.1d