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)

In order to study the role of the renin-angiotensin system in patients with diabetic nephropathy, renin release and the juxtaglomerular apparatus were studied in 17 diabetic patients with proteinuria and in 23 without proteinuria; 8 normal subjects were used for conctrls. Despite hypertension and marked arteriosclerosis, plasma renin activity (supine posture) was normal; however, the renin response to salt restriction and upright posture was less in the diabetic patients with proteinuria than in the controls. Renal renin content, determined at autopsy, was also normal. Examination of the juxtaglomerular apparatus in the diabetic patients with proteinuria revealed hyalinization of the afferent and efferent arterioles in most of the glomeruli and various degrees of destruction of the juxtaglomerular cells. The findings suggest that renin production is not increased in diabetic patients with proteinuria plus marked vascular damage, and that the renin-angiotensin system in patients with diabetic nephropathy apparently does not play an important role in the exacerbation of hypertension or the degree of vascular damage.
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PMID:Renin and the juxtaglomerular apparatus in diabetic nephropathy. 61 49

The results of 2 studies to determine the relationship between hormonal contraceptive (h.c.) use, hypertension, and nephritis are reported. 828 women, 16-50 years of age, were divided into 3 groups. 1 group had never used h.c.s., 1 group was presently using h.c.s., and 1 group had used h.c.s. for the last time more than a year prior to the study. Women 26-35 years of age who were using h.c.s. at the time of the study more often developed hypertension than other groups. The h.c. users who developed hypertension more often had a family history of hypertension or diabetes mellitus, more often had diabetes themselves, and more often suffered from preeclampsia or eclampsia during pregnancy. In a second study, ethinyl estradiol, norethisterone acetate, epsilon aminocapronic acid, desoxycorticosterone acetate, and table salt were administered singly or in combinations to 2 groups of rats. In one group, a Goldblatt-type hypertension was induced with a clamp on the nephric artery. No increase in blood pressure was observed in animals which received only an estrogenic or progestagenic agent. Significant increases in blood pressure were observed in animals that were given combinations of estrogenic and progestagenic agents, however. Significantly increased plasma-resin activity was observed in all animals which were given estrogen, while animals receiving desoxycorticosterone acetate showed a highly significant decrease in plasma-renin activity.
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PMID:[Oral contraceptives, hypertension and nephrosclerosis]. 62 80

Nineteen patients with hypertension in whom all known causes of blood pressure elevation had been ruled out were classified as "salt-sensitive" or "nonsalt-sensitive" from the changes in blood pressure with changes in sodium intake from 9 meq to 249 meq/day. With the diet containing 249 meq sodium per day, there were no statistically significant differences in plasma sodium, potassium, chloride, aldosterone, cortisol or renin activity, or in urinary potassium, aldosterone or 17-hydroxycorticosteroids between the two groups. The "salt-sensitive" patients retained more sodium on the high-sodium diet than did the patients who were not sensitive to salt ("nonsalt-sensitive"); accordingly, sodium induced more weight gain in the salt-sensitive patients.
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PMID:The effect of high-sodium and low-sodium intakes on blood pressure and other related variables in human subjects with idiopathic hypertension. 62 67

The effect of total adrenalectomy on the mechanisms of arterial pressure control was studied in uninephrectomized rats with and without renal artery stenosis (Goldblatt one-kidney model). Four groups of rats were prepared and maintained on high-salt intake (1% NaCl): uninephrectomized-KI; KI + adrenalectomy-KIAx; uninephrectomized with renal artery stenosis-GI; and GI with adrenalectomy-GIAx. Over 3 wk blood pressure rose significantly in both GI and GIAx but the degree of increase in GI was greater. Hyponatremia, hyperkalemia, and increased plasma urea nitrogen were observed in both KIAx and GIAx. Plasma renin concentration (PRC) and plasma renine activity (PRA) were markedly increased and plasma renin substrate (PRS) was decreased in both adrenalectomized groups. Infusion of saralasin resulted in significant and similar reductions in mean arterial pressure (MAP) in KIAx and GIAx, but had no effect on MAP in KI and GI. These results allow approximations of the contribution to total MAP of identifiable components, which are: the total adrenal component, the renin-angiotensin system component, which partially compensates for loss of the adrenal secretions, and the independent effect of the renal artery clip. Thus, a multifactorial analysis of GI hypertension is provided.
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PMID:Adrenal gland in experimental renal hypertension. 62 42

We have studied the effects of intravenous infusion of saralasin, a competitive antagonist of angiotensin II, in 27 hypertensive patients: 13 had essential hypertension, 14 had renal lesions which involved the renal artery in 9 cases. In essential hypertensives saralasin administration did not significantly lower blood pressure, even after mild salt depletion. It induced a decrease in blood pressure in 7 patients with renal abnormalities (5 with renal artery stenosis, 2 with unilateral parenchymal disease). It may be suggested that in these cases hypertension was dependent, at least partly, on the renin-angiotensin system. In agreement with other investigators, we have found a relationship between the level of plasma renin activity and the blood pressure decrease obtained by saralasin. In patients with unilateral renal artery stenosis, blood pressure decrease was related to renal vein ratio of plasma renin activity.
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PMID:[Clinical usefulness of saralasin in human hypertension (author's transl)]. 64 79

It was shown in experiments on dogs that intravenous injection of adrenaline or noradrenaline in a dose of 2 microgram/kg per min was accompanied by an increase of resistance of the renal vessels with unchanged general renal circulation, and administration of adrenaline against the background of obsidan action--by an increase of resistance and reduction of blood flow, and--against the background of phentholamine action--by a reduction of resistance with unchanged circulation. On the basis of these data and those obtained by the author earlier a supposition is put forward on a possible mechanism of a combination of functions in the systems of circulation and excrection in the control of general water-salt homeostatis in extraordinary hemodynamic shifts with the participation of the humoral factor--renin-angiotensine system.
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PMID:[Variants in the catecholamine effect on renal hemodynamics]. 64 38

The mechanism by which the angiotensin converting enzyme inhibitor, teprotide (SQ 20881), lowers blood pressure was assessed in anesthetized normotensive and spontaneously hypertensive (SHR) rats. Teprotide always was administered at a maximally effective dose of 1 mg/kg. In six normal Wistar rats, teprotide lowered blood pressure only after sodium depletion, an effect which was abolished by bilateral nephrectomy. Saralasin infusion (5 microgram/kg/min) into salt-depleted normal rats induced a blood pressure effect similar to that of teprotide. When administered in addition to saralasin infusion, teprotide did not reduce blood pressure further in normal rats or in SHR. When blood pressure of normal rats was raised by angiotensin II infusion (200 ng/kg/min), teprotide did not affect the induced blood pressure increase. In contrast, the pressure rise induced by angiotensin I infusion (230 ng/kg/min) was reversed by saralasin, but again concomitant administration of teprotide did not induce further blood pressure reduction. Thus, under the particular conditions of the present study, teprotide did not appear to exert its hypotensive effect by any mechanism other than inhibition of the renin-angiotensin system. Furthermore, given at a maximally effective dose to the rat, it produced no greater vasodepressor effect than did saralasin.
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PMID:Mechanism of blood pressure reduction by teprotide (SQ 20881) in rats. 65 Nov 28

1. Chronic ligation of the bile duct in dogs is associated with salt retention and a blunted natriuretic response to extracellular volume expansion. The mechanism of this phenomenon has not been clarified. 2. We have examined the influence of chronic beta-adrenergic blockade on sodium excretion in dogs with bile-duct ligation during extracellular hypotonic volume expansion. 3. Urinary excretion of sodium and fractional excretion of sodium rose significantly after 5 days of oral DL-propranolol administration to dogs with bile-duct ligation. 4. The antinatriuresis after bile-duct ligation was not followed by a significant alteration in the mean peripheral plasma renin activity as compared with control values. 5. It is suggested that propranolol can partially reverse the antinatriuresis of chronic bile-duct ligation, and that this is mediated by an extrarenal effect of the beta-adrenergic blockade.
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PMID:Natriuretic effect of propranolol on dogs with chronic bile-duct ligation. 65 28

A newborn boy (birth weight 2550 g) presented from the first days of life with poor drinking, moderate vomiting and persistent weight loss. On hospital admission at age 4 weeks, there were severe dehydration, dystrophy and electrolyte disturbances (Na 107, Cl 80, K 5,4 mval/l). The usual causes of salt wasting were excluded, but plasma renin activity, plasma aldosterone and urinary aldosterone-18-glucuronide were markedly increased. DOCA had no salt-retaining effect, but a sodium chloride supplement of 3 g per day improved the clinical condition dramatically and normalized the electrolyte values. With this treatment, plasma renin activity and aldosterone were normal or almost normal beyond the age of 6.5 months, but urinary aldosterone-18-glucuronide remained slightly increased. Considerable augmentation of the plasma renin activity and of urinary aldosterone-18-glucuronide, but no clear salt loss were induced by spironolactone. With salt restriction, there was evidence for marked salt loss. Its progress could be inhibited by administration of indomethacin. Since indomethacin inhibits the synthesis of prostaglandins with saluretic activity, it is probable that the prostaglandins participate in the pathogenesis of the salt wasting in pseudohypoaldosteronism.
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PMID:Congenital pseudohypoaldosteronism: case report and review. Effect of indomethacin during sodium chloride depletion. 65 59

The role of the renin-angiotensin system in the regulation of the systemic and coronary circulations during sodium depletion was studied in conscious normotensive dogs by i.v. administration of teprotide (0.5 mg/kg), an angiotensin-converting enzyme inhibitor, and saralasin (0.05-5 mug/kg per min), an angiotensin-receptor antagonist. Sodium depletion was produced by administering a low sodium diet and furosemide for 5 days. Administration of both teprotide and saralasin lowered systemic arterial blood pressure and total peripheral vascular resistance. Simultaneously, cardiac output increased, but left ventricular end-diastolic pressure, dP/dt, and dP/dt/P did not change significantly. Furthermore, both agents reduced diastolic coronary vascular resistance and increased coronary blood flow, but did not affect myocardial oxygen consumption, left ventricular work, or myocardial efficiency. These systemic and coronary vasodilator effects of teprotide and saralasin, however, were not observed in normal dogs on a regular sodium diet; in this group, the only effect noted was a slight increase in arterial pressure during saralasin infusion. Arterial plasma concentration of norepinephrine did not differ between normal and sodiumdepleted dogs, nor did it change significantly after teprotide administration. These results suggest that, during salt depletion, angiotensin II exerts an active vasoconstrictor action on the systemic and coronary vessels, but has no significant effects on myocardial contractility or energetics. It also appears likely that the increase in cardiac output observed in sodiumdepleted dogs after angiotensin inhibition was caused, at least in part, by the decrease in systemic arterial pressure.
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PMID:Renin-angiotensin system inhibition in conscious sodium-depleted dogs. Effects on systemic and coronary hemodynamics. 65 80


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