Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The place of captopril (C) testing in the screening for renovascular hypertension is still controversial. Baseline and C-stimulated plasma renin concentrations (PRC) were measured in 113 hypertensives, who where referred for the exclusion of secondary hypertension. In addition intravenous digital subtraction angiography (DSA) and a renal scintigraphy were performed. When renal artery disease was revealed by DSA or renin was stimulated the renal arteries were visualized by direct arteriography (and treated by angioplasty if possible). 86 patients underwent each diagnostic test: 21% had renovascular hypertension. Unilateral renal artery stenosis (n = 10) was detected by the captopril test (cutoff values: baseline greater than 40 microU/ml, after C greater than 180 microU/ml, sensitivity 100%). Bilateral renal artery stenosis (n = 8) was missed when the disease was equally severe on either side (sensitivity 50%). The specificity of C testing was 82%, overall sensitivity (uni- and bilateral disease 78%, prevalence 21%, predictive value of the positive test 0.56, predictive value of the negative test 0.93). With i.v.-DSA the renal arteries were technically evaluable in 91% (82/92) of cases. The sensitivity for the detection of all renal artery stenoses was 79% (uni-lateral 100%, bilateral 40%, specificity 97%). The sensitivity of renal scintigraphy for the detection of unilateral renal artery stenoses was 50%, for the detection of bilateral renal artery stenoses 43%, specificity 81%. The present study demonstrates the usefulness of captopril for the detection of unilateral renal artery stenosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Status of the captopril test in the diagnosis of hypertension]. 268 53

Seventy-two patients, aged 6-69 years, were operated on because of presumed renovascular hypertension and subjected to follow-up studies for 4-60 months (mean 28). Unilateral renal artery stenosis was present in 47 patients. Surgery was followed by normalization of blood pressure (BP) in 28 and improvement in 7, whereas 12 showed no response. Sixteen were below the age of 40 and only one failed to respond to surgery. Peripheral venous plasma renin activity (PRA) was increased in 32 and urinary aldosterone elevated in 22 of 35 patients responding favourably to surgery. Renal vein PRA was higher from the kidney with the stenotic renal artery as compared to the contralateral side in all patients responding to surgery. Preoperative peripheral PRA difference was also found in 7 of 12 patients not responding to surgery. Preoperative peripheral PRA was increased in 26 of the patients becoming normotensive after surgery. In 20 of these patients normalization of BP was associated with a fall in peripheral PR. Twenty-five patients had bilateral renal artery stenosis. Four of them had severe hypertension, renal insufficiency and generalized atherosclerosis. They died in immediate connection with operation. Unilateral operation, performed in 11 of the remaining 21 patients, was followed by normalization of BP in 3 and no response in 8. Bilateral reconstructive surgery, performed in 10 patients, resulted in normotension in 2 and improvement in 7. Our studies indicate that determination of peripheral PRA and/or urinary aldosterone can serve as a useful prognostic indicator after surgery in hypertensive patients with renal artery stenosis.
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PMID:Pre- and postoperative studies in 72 hypertensive patients with renal artery stenosis, with special reference to renin activity and aldosterone. 703 32

Unilateral renal artery stenosis can lead to a non-functional kidney which secretes large amounts of renin. Four cases are presented in which the high renin state resulted in hypertension, proteinuria from the intact contralateral kidney, and secondary aldosteronism. The proteinuria was in the nephrotic range, which is unusual in renovascular hypertension, but gradually disappeared after correction of the high renin state by removal of the renin-secreting kidney or administration of an ACE inhibitor. Accordingly, when there is marked proteinuria in the presence of new-onset or rapidly progressive hypertension, hypokalaemic alkalosis, and a high peripheral PRA, renal artery stenosis should be considered since the proteinuria may be reversible after nephrectomy, repair of the ischaemic kidney or medical therapy.
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PMID:Reversible nephrotic syndrome due to high renin state in renovascular hypertension. 773 87

Connexins (Cxs) are a family of transmembrane proteins that form gap junctions with unique and redundant biophysical functions. Juxtaglomerular cells express Cx40, which is crucial to the control of renin secretion by blood pressure and angiotensin II, and mice that lack Cx40 have high plasma renin and hypertension. To examine whether normal juxtaglomerular cell function depends on the unique properties of Cx40, we measured renin release in mice where the coding sequence for Cx40 was replaced by that for Cx45, using the knock-in method. We first found that the knock-in strategy indeed resulted in expression of Cx45 but not Cx40 in the juxtaglomerular cells of these mice. The plasma renin concentration of the knock-in mice was similar to that in wild-type mice. The high blood pressure of the Cx40 knockout mice was significantly reduced when Cx45 was knocked into the locus but remained mildly elevated compared to wild-type mice. Blockade of angiotensin II formation by enalapril increased the plasma renin concentration in wild-type and the Cx45 knock-in mice but not in the Cx40 knockout mice. Infusion of angiotensin II into isolated perfused kidneys results in decreased renin release, a phenomenon that was attenuated in the Cx40 knockout mice. However, in the Cx45 knock-in mice, angiotensin II suppressed renin release similar to its effect in wild type mice. Unilateral renal artery stenosis increased the plasma renin concentration and blood pressure in both the wild-type and the Cx45 knock-in mice but not in the Cx40 knockout mice. Since Cx40 can be replaced by Cx45, a connexin with a significantly lower conductivity, we suggest that the regulation of renin release is not dependent on the unique electrical properties of these channel proteins.
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PMID:Substitution of connexin40 with connexin45 prevents hyperreninemia and attenuates hypertension. 1921 2

The salt intake of an organism controls the number of renin-producing cells in the kidney by yet undefined mechanisms. This study aimed to assess a possible mediator role of preglomerular blood pressure in the control of renin expression by oral salt intake. We used wild-type (WT) mice and mice lacking angiotensin II type 1a receptors (AT(1a)-/-) displaying an enhanced salt sensitivity to renin expression. In WT kidneys, we found renin-expressing cells at the ends of all afferent arterioles. A low-salt diet (0.02%) led to a moderate twofold increase in renin-expressing cells along afferent arterioles. In AT(1a)-/- mice, lowering of salt content led to a 12-fold increase in renin expression. Here, the renin-expressing cells were distributed along the preglomerular vascular tree in a typical distal-to-proximal distribution gradient which was most prominent at high salt intake and was obliterated at low salt intake by the appearance of renin-expressing cells in proximal parts of the preglomerular vasculature. While lowering of salt intake produced only a small drop in blood pressure in WT mice, the marked reduction of systolic blood pressure in AT(1a)-/- mice was accompanied by the disappearance of the distribution gradient from afferent arterioles to arcuate arteries. Unilateral renal artery stenosis in AT(1a)-/- mice on a normal salt intake produced a similar distribution pattern of renin-expressing cells as did low salt intake. Conversely, increasing blood pressure by administration of the NOS inhibitor N-nitro-l-arginine methyl ester or of the adrenergic agonist phenylephrine in AT(1a)-/- mice kept on low salt intake produced a similar distribution pattern of renin-producing cells as did normal salt intake alone. These findings suggest that changes in preglomerular blood pressure may be an important mediator of the influence of salt intake on the number and distribution of renin-producing cells in the kidney.
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PMID:Role of blood pressure in mediating the influence of salt intake on renin expression in the kidney. 2235 14

The renin-angiotensin-aldosterone system and cardiac natriuretic peptides [atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP)] are opposing control mechanisms for arterial blood pressure. Accordingly, an inverse relationship between plasma renin concentration (PRC) and ANP exists in most circumstances. However, PRC and ANP levels are both elevated in renovascular hypertension. Because ANP can directly suppress renin release, we used ANP knockout (ANP(-/-)) mice to investigate whether high ANP levels attenuate the increase in PRC in response to renal hypoperfusion, thus buffering renovascular hypertension. ANP(-/-) mice were hypertensive and had reduced PRC compared with that in wild-type ANP(+/+) mice under control conditions. Unilateral renal artery stenosis (2-kidney, 1-clip) for 1 wk induced similar increases in blood pressure and PRC in both genotypes. Unexpectedly, plasma BNP concentrations in ANP(-/-) mice significantly increased in response to two-kidney, one-clip treatment, potentially compensating for the lack of ANP. In fact, in mice lacking guanylyl cyclase A (GC-A(-/-) mice), which is the common receptor for both ANP and BNP, renovascular hypertension was markedly augmented compared with that in wild-type GC-A(+/+) mice. However, the higher blood pressure in GC-A(-/-) mice was not caused by disinhibition of the renin system because PRC and renal renin synthesis were significantly lower in GC-A(-/-) mice than in GC-A(+/+) mice. Thus, natriuretic peptides buffer renal vascular hypertension via renin-independent effects, such as vasorelaxation. The latter possibility is supported by experiments in isolated perfused mouse kidneys, in which physiological concentrations of ANP and BNP elicited renal vasodilatation and attenuated renal vasoconstriction in response to angiotensin II.
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PMID:Natriuretic peptides buffer renin-dependent hypertension. 2471 31