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

Atrial natriuretic peptide is a recently discovered cardiac hormone with natriuretic, vasodilatory and hypotensive activities. The role of this hormone in the pathophysiology of hypertension is of particular interest. In contrast to an earlier concept, a deficiency of the atrial peptide could not be found in animal models of hypertension or in patients. ANP plasma levels were elevated in SHR with accelerated hypertension, in salt-sensitive Dahl rats, in rats with DOCA-salt-hypertension and in animals with renovascular hypertension. Elevated ANP levels under these conditions can be explained by an expansion of the intravascular volume or by an elevated atrial wall stretch induced by the hypertension itself. In patients with primary hypertension, plasma levels of the peptide are raised in some patients and are normal in others. Plasma ANP levels correlate with age, blood pressure and signs of left ventricular hypertrophy. A negative correlation is described between ANP and renin. Measurement of plasma ANP levels does not allow a differentiation between primary and secondary forms of hypertension. Elevated ANP levels are also found in primary hyperaldosteronism and in renal failure. Stimulation of ANP secretion by physical exercise and dietary salt loading is maintained in hypertension. Infusion of 1-28-hANP leads to a reduction in systemic arterial pressure in normotensives and hypertensives. The natriuresis induced by exogenous ANP is more pronounced in hypertensives. Stimulation of endogenous ANP secretion does not prevent the rise in blood pressure possibly due to a reduction in ANP receptors in target tissues.
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PMID:[Atrial natriuretic peptide and its significance for arterial hypertension]. 253 Dec 53

Na+-K+-ATPase activity and [3H]ouabain binding were studied in cardiac ventricles of single wrapped kidney and DOCA-NaCl hypertensive rats. It was found that the total Na+-K+-ATPase activity decreased in the DOCA-NaCl and kidney wrapped hypertensive rats. The decrease of enzyme activity in DOCA-NaCl hypertensive rats was due to extracellular fluid expansion induced by NaCl loading, as DOCA itself had no effect on the enzyme. All these alterations were specific for Na+-K+-ATPase, since Mg2+-ATPase and 5'-nucleotidase activities were unaffected. Binding studies with [3H]ouabain showed that the decrease in Na+-K+-ATPase activity was due to a reduction in the number of binding sites for ouabain rather than to a change of binding affinity. The reduced myocardial Na+-K+-ATPase activity observed in these two types of low renin hypertension, coupled with the observation of reduced vascular Na+ pump activity by others, suggests a common underlying defect in the cardiovascular Na+-K+ transport system of these hypertensive rats.
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PMID:Myocardial Na+-K+-ATPase activity and [3H]ouabain binding sites in hypertensive rats. 255 24

The effects of K+-canrenoate, a digoxin antagonist, on the role of digoxin-like factor in the development of DOCA-salt hypertension has been examined. DOCA-salt rats treated with 66 mg kg-1 day-1 of K+-canrenoate (s.c.) presented a lower increase in blood pressure (P less than 0.01), less cardiac hypertrophy (P less than 0.05) and hypokalaemia (P less than 0.05) than non-treated DOCA-salt rats. K+-canrenoate treatment did not lead to significant changes in urinary volume, Na+ and K+ urinary excretion or suppression of plasma renin activity in DOCA-salt rats. None of the parameters were significantly different between uninephrectomized-salt rats treated or non-treated with K+-canrenoate. These data suggest a role for digoxin-like factor in DOCA-salt hypertension. However, the non-normalization of blood pressure observed in K+-canrenoate DOCA-salt treated rats indicates that other factors contribute to the initiating mechanisms in this type of hypertension. Moreover, these data suggest that digoxin-like factor plays no role in the suppression of plasma renin activity induced by DOCA and salt treatment.
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PMID:Effects of K+-canrenoate on the development of DOCA-salt hypertension. 256 21

1. DOCA and 9 alpha-fludrocortisone were given to mice on a high-sodium diet for periods of up to 20 weeks, resulting in decreases in plasma renin concentration, renal renin concentration and renal renin mRNA with both treatments. 2. Plasma renin concentration was suppressed prior to suppression of renin mRNA and renal renin levels, indicating that suppression of synthesis and secretion of renin occur separately. 3. The decrease in renal renin concentration that occurred with DOCA was greater and more rapid than the decrease that occurred with 9 alpha-fludrocortisone, suggesting that DOCA caused intra-renal breakdown of renin. 4. When DOCA was given to mice on a low-sodium diet, plasma renin concentration and renal renin concentration increased, indicating that the effects of DOCA on renin levels were dependent on dietary sodium. 5. Renin secretion and synthesis appeared to be controlled by different mechanisms and sodium balance has an important effect on both processes.
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PMID:Effect of mineralocorticoids and salt loading on renin release, renal renin content and renal renin mRNA in mice. 267 70

Two patients with hypermineralocorticoidism due to deoxycorticosterone (DOC) excess are described. The plasma 17-deoxysteroids of the zona fasciculata (ZF), namely DOC, corticosterone, 18-hydroxydeoxycorticosterone, and 18-hydroxycorticosterone, were elevated. Plasma androgen concentrations were normal, and plasma aldosterone and renin levels were low. One patient, who had benign adrenocortical adenoma, had normal plasma cortisol levels. The other patient, who had metastatic adrenocortical carcinoma, had low plasma cortisol, presumably due to elevated plasma corticosterone levels. While tumors producing only 17-deoxysteroids are rare, they have provided new insights into the regulation of 17-deoxysteroid secretion by the ZF. Presumptive suppression of a non-ACTH factor by adenoma-produced DOC transiently impaired the early postoperative responses to ACTH of the ZF 17-deoxysteroids of the contralateral adrenal. The dissociation of 17-deoxysteroids from cortisol in normal subjects given either dexamethasone or DOC acetate provides additional evidence for such a factor.
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PMID:Pathophysiology of deoxycorticosterone-secreting adrenal tumors. 282 55

To provide information on the possible influence that hypertension or its treatment might have on the development of cysts in autosomal dominant polycystic kidney disease, we studied the effects of the sodium content of the diet, DOCA-salt hypertension, renovascular hypertension, and the administration of enalapril or furosemide on the development of 2-amino-4-5-diphenylthiazole (DPT)-induced renal cystic disease. DOCA-salt hypertension caused vascular and glomerular lesions and proteinuria, but it did not enhance the development of cysts. Cytogenesis was enhanced in experimental conditions where the renin-angiotensin system is known to be activated. On the other hand, interventions known to suppress the renin-angiotensin system lessened the development of cysts. We hypothesize that this effect might be mediated by intrarenal angiotensin II and its capacity to promote cell growth and to control the postglomerular vascular resistances and the compliance of the renal interstitium.
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PMID:Mechanisms affecting the development of renal cystic disease induced by diphenylthiazole. 284 32

Atrial natriuretic factor or peptide (ANP) is a peptide recently isolated from mammalian atria with potent natriuretic, vasorelaxant, and aldosterone-inhibitory properties. ANP may play an important role in the regulation of blood pressure and body salt and fluid balance. The presence of binding sites for ANP in the vasculature and adrenal glomerulosa of rats and in platelets in humans has been demonstrated. These sites are involved in the mediation of the vasorelaxant effect of ANP and its inhibitory action on aldosterone secretion. The role of binding sites on platelets is unknown, but the availability of platelets makes them a useful model for investigating the regulation of receptors for atrial natriuretic factor in humans. The effect of sodium depletion and loading and mineralocorticoids on the density of rat vascular and adrenal sites for ANP was examined, as well as changes that occur after development of renovascular and DOCA-salt hypertension in rats. Sodium loading in the presence of reduced renal mass (unilateral nephrectomy) or mineralocorticoid administration produced renin suppression and resulted in down-regulation of vascular ANP receptors. In one-kidney, one-clip Goldblatt hypertensive rats and in DOCA-salt hypertensive rats, two models of volume-expanded, non-renin-dependent experimental hypertension, the density of ANP binding sites in the mesenteric arterioles was significantly decreased. The sensitivity to ANP of precontracted aorta from renovascular and mineralocorticoid hypertensive rats was significantly reduced. No consistent changes occurred in the density of ANP binding sites in the adrenal glomerulosa.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of receptors for atrial natriuretic peptide in the rat and human. 285 69

The autonomic and antihypertensive activities of amosulalol (YM-09538) were studied in conscious rats. Single oral administration of amosulalol antagonized the phenylephrine-induced pressor and isoproterenol-induced positive chronotropic responses with DR10 values of 11.5 and 13.6 mg/kg in pithed rats, respectively, indicating that the compound inhibits both alpha 1- and beta 1-adrenoceptors to almost the same extent in agreement with previously reported results in vitro. Amosulalol was approximately 50 times less potent than prazosin and 12 times more potent than labetalol at alpha 1-adrenoceptors, and it was approximately as effective as labetalol and 2 times more potent than propranolol at beta 1-adrenoceptors. In spontaneously hypertensive rats (SHR), renal hypertensive rats and DOCA/salt hypertensive rats, a single oral administration of amosulalol (3-30 mg/kg) lowered acutely systolic blood pressure with a duration of over 6 hr and was found to be approximately 50 times less potent than prazosin and 3 times more potent than labetalol in lowering blood pressure. Propranolol did not cause such an immediate hypotensive effect. Amosulalol and labetalol did not increase heart rate, whereas prazosin induced a tachycardia in the hypertensive rats. Repeated oral administrations of amosulalol and labetalol (50 mg/kg/day, b.i.d., for 12 weeks) produced not only an antihypertensive effect without evidence of tolerance, but also reductions in plasma renin activity (PRA) and heart rate in SHR with established hypertension. We conclude that alpha-adrenoceptor blockade by amosulalol might account for its antihypertensive activity and that its beta-adrenoceptor blockade might inhibit reflexogenic increases in heart rate and PRA due to the reduction in blood pressure.
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PMID:Autonomic and antihypertensive activity of oral amosulalol (YM-09538), a combined alpha- and beta-adrenoceptor blocking agent in conscious rats. 286 2

Instrumented normotensive and two-kidney, one clip Goldblatt hypertensive dogs were placed on normal salt, high salt and DOCA-salt regimens and the effect on mean arterial blood pressure (MAP) and iliac vascular resistance (IVR) determined. High salt and DOCA-salt did not alter these variables in the Goldblatt hypertensive group. DOCA-salt increased MAP in the normotensives by 12 mmHg; however, IVR was not significantly increased by this treatment. In order to determine the degree of sympathetic tone in the iliac vascular bed, the change in IVR evoked by the alpha 1-adrenoceptor antagonists, urapidil and prazosin, was assessed. There were similar reductions in MAP and IVR after alpha 1-blockade in both groups of dogs, regardless of the salt regimen. However, urapidil caused a greater decrease in MAP in the normotensives than in the hypertensives. Captopril administration after alpha 1-blockade caused further reductions in MAP and IVR in the hypertensives, and in the MAP of the normotensive dogs on normal or high salt, indicating that the renin-angiotensin system maintained blood pressure in these groups. These results suggest that sympathetic tone is not increased by high salt- or DOCA-salt in normotensive or Goldblatt hypertensive dogs for the 8-11 day duration of these treatments.
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PMID:Effect of alpha 1-adrenoceptor blockade on blood pressure and iliac vascular resistance in normotensive and Goldblatt hypertensive dogs; influence of dietary salt and DOCA-salt. 288 79

The effects of converting enzyme inhibition on the cardiac mass, isomyosins polymorphism, and collagen network in the left ventricle have been studied in renovascular, hypertensive, spontaneously hypertensive, and normotensive rats. The isoenzyme profile of left ventricular myosins was used as an indirect marker of the intrinsic property of contractility, whereas the collagen network, measured by a morphometric method, represented an indirect structural marker of the arrhythmogenic risk. One-clip, two-kidney renovascular hypertension was associated with cardiac hypertrophy, a shift in the isomyosin profile, and accumulation of collagen within the left ventricular myocardium. In this renin-angiotensin-dependent model, one month of treatment with converting enzyme inhibitor normalized blood pressure and consistently reversed cardiac hypertrophy and the isomyosin profile. Converting enzyme inhibitor treatment of 12-week-old spontaneously hypertensive rats for three months significantly decreased blood pressure but did not completely normalize it. The increase in cardiac mass observed in spontaneously hypertensive rats was not reversed by this short treatment. Nevertheless, the percentage of the V1 form of myosin increased slightly after treatment, and the collagen content of the left ventricle was considerably decreased. Converting enzyme inhibition did not decrease blood pressure in DOCA-salt hypertension, and no changes were observed in cardiac hypertrophy, isomyosin profile, or the collagen network. The cardiac hypertrophy that occurs with aging in normotensive rats was associated with a significant shift in isomyosin profile and a large accumulation of collagen. Thus, aging mimics several of the quantitative and qualitative changes in the left ventricular protein profile observed in hypertension. In young normotensive rats, converting enzyme inhibition significantly decreased blood pressure and left ventricular mass, increased the percentage of V1 isomyosin, and prevented the accumulation of collagen. In one-year-old normotensive rats, treatment for six months with converting enzyme inhibitor decreased blood pressure, decreased cardiac mass, and prevented the accumulation of collagen; the isomyosin profile was not modified. Converting enzyme inhibition, by acting on cardiac afterload, can bring about quantitative and qualitative changes in the cardiac proteins of both hypertensive and normotensive rats.
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PMID:Myocardial effect of converting enzyme inhibition in hypertensive and normotensive rats. 297 59


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