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)

This study was undertaken to explore the effects of chronic low-level cadmium ingestion in Dahl hypertension-resistant (R) and hypertension-sensitive (S) lines of rats. Groups of weanling female R and S rats were given 0 or 1 mg cadmium/1. in drinking water and fed either a low salt (0.4% NaCl) or a high salt (4% NaCl) diet for 28 weeks. Cadmium produced hypertension associated with gross cardiac hypertrophy and mild to moderate renal vascular changes in S, but not in R, rats on a low salt diet. Cadmium enhanced the rate and degree of development of salt-induced hypertension without exacerbating the hypercholesterolemia or renal vascular lesions normally observed in S rats on a high salt diet. Cadmium lowered circulating cholesterol levels in both lines on a low salt diet. Cadmium had no influence on growth, blood urea nitrogen concentration, plasma renin activity, tumor formation, or survivorship in R and S rats on either salt diet. This study indicates that the genetic composition is a critical determinant of the adverse effects of chronic low-level cadmium ingestion in rats. In addition to the experimental implications, these findings may have relevance to the problem of human "essential" hypertension.
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PMID:Effects of cadmium ingestion in rats with opposite genetic predisposition to hypertension. 48 40

The effect of spironolactone (50 mg b.i.d.) in essential hypertension was studied by measurement of effective renal plasma flow (ERPF), blood urea nitrogen (Ur+), serum creatinine (Cr), cardiac index (CI), plasma volume (PV), body weight (BW), mean arterial blood pressure (MAP), total peripheral resistance index (TPRI), plasma renin activity (PRA) and plasma aldosterone (PA) in two groups of patients. Ten cases had determinations before, after 5 weeks and 4 months of treatment; fourteen cases who had been treated at an average of 18 months, had measurements while on treatment and 5 weeks after cessation of the drug. Among the ten patients ERPF fell in six and increased in four patients during treatment, but was statistically unchanged in the total group. Ur + and Cr were also unchanged by treatment. ERPF was unchanged after withdrawal of the drug. During treatment BW decreased 3.5%, PV decreased in nine and increased in one patient, while PRA and PA increased 426% and 202%, respectively. After cessation of the aldosterone blockade, BW increased 1.9%, PV 10.5% while PRA and PA fell 60% and 48.9%, respectively. MAP fell in eight out of ten patients during treatment. This fall was associated with a fall in CI or TPRI, or both. After withdrawal of the drug, MAP increased in nine and decreased in five of the patients. The data shows that this dosage of spironolactone gave minor adjustments of the systemic and renal circulation in spite of the consistent changes in BW, PV, PRA and PA.
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PMID:Haemodynamic effects of treatment and withdrawal of spironolactone in essential hypertension. 52 64

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

Transient hypertension occurred in 3 patients shortly after blunt injury to the abdomen. Renal trauma was suspected in all 3 patients and radiological evidence for renal injury was present in 2. Plasma renin activity definitely was elevated in 1 patient and probably was elevated in another. There was a decrease in blood pressure in all 3 patients during infusion of the angiotensin II analogue--saralasin--showing that the hypertension in these patients was angiotensin-mediated. Renal function as reflected by the blood urea nitrogen, creatinine and electrolytes was not impaired significantly. Thus, acute hypertension after blunt abdominal trauma may be angiotensinogenic and is not necessarily sustained.
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PMID:Renin angiotensin involvement in transient hypertension after renal injury. 65 Jul 71

Eight men, 19-35 years of age, breathed 20.9% (normal oxygen), 13.9% (mild hypoxia) or 11.1% (severe hypoxia) oxygen in nitrogen gas mixtures during three 20 min periods, which were separated by 1 h recovery periods. The order in which the gas mixtures were breathed was random. The partial pressure of oxygen decreased from a mean of 93.5 during exposure to normal oxygen to 53.9 and 36.7 mmHg during mild and severe hypoxia respectively. There were corresponding decreases in haemoglobin saturation. The partial pressure of carbon dioxide was lower and the pH higher during severe hypoxia than during exposure to normal oxygen. There were no changes in the plasma osmolality or in the concentrations of sodium or potassium in the plasma. There was a tendency for both the renin activity and the concentration of aldosterone in the plasma to decrease progressively as the percentage of oxygen breathed decreased. Unlike severe hypoxia, mild hypoxia suppressed the concentration of antidiuretic hormone (ADH) in the plasma of all subjects by about 59%; during severe hypoxia the reduction was not significant, being only about 33%. These data are consistent with the suggestion that the effect of hypoxia on the release of ADH is dependent on the level of hypoxia.
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PMID:Response of antidiuretic hormone to acute exposure to mild and severe hypoxia in man. 66 35

The antihypertensive effect of spironolactone was studied in 20 patients with essential hypertension and normal stimulated peripheral renin activity (PRA). Single-blind 8-wk treatment periods of placebo, 100, 200, and 400 mg spironolactone were used in consecutive order. Average supine and erect blood pressures were lower than placebo values at the end of each treatment. A prominent orthostatic effect was observed. Changes in blood pressure were not related to changes in body weight, PRA, or blood urea nitrogen. A larger proportion (50%) of patients had a more normal erect diastolic pressure at the end of 400 mg/day than at the end of 100 mg/day (20%), but the response to 400 mg/day could not be predicted from the responses to lower doses. Larger doses of spironolactone were predictably associated with rises in serum potassium, PRA, and aldosterone excretion. Adverse effects were absent during therapy with 100 mg/day but were frequent during 200--400 mg/day. Although there are no apparent advantages in increasing spironolactone from 100 to 200 mg/day in this group of patients with normal renin hypertension, increasing the dose to 400 mg/day resulted in better blood pressure control with more frequent adverse effects.
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PMID:Antihypertensive responses to spironolactone in normal renin hypertension. 69 76

The role of the renin-angiotensin system in mediating the circulatory and metabolic responses to hypoxia was studied in three groups of conscious dogs that were infused continuously with normal saline, teprotide (10 mug/kg per min), and saralasin (1 mug/kg per min), respectively. Hypoxia was produced by switching from breathing room air to 5 or 8% oxygen-nitrogen mixture. Plasma renin activity increased from 2.3+/-0.4 to 4.9+/-0.8 ng/ml per h during 8% oxygen breathing, and from 2.8+/-0.4 to 8.4+/-1.8 ng/ml per h during 5% oxygen breathing. As expected, cardiac output, heart rate, mean aortic blood pressure, and left ventricular dP/dt and dP/dt/P increased during both 5 and 8% oxygen breathing in the saline-treated dogs; greater increases occurred during the more severe hypoxia. Teprotide and saralasin infusion diminished the hemodynamic responses to 5% oxygen breathing, but did not affect the responses to 8% oxygen breathing significantly. In addition, the increased blood flows to the myocardium, kidneys, adrenals, brain, intercostal muscle, and diaphragm that usually occur during 5% oxygen breathing were reduced by both agents. These agents also reduced the increases in plasma norepinephrine concentration during 5% oxygen breathing, but had no effects on tissue aerobic or anaerobic metabolism. In dogs pretreated with propranolol and phentolamine, administration of teprotide (0.5 mg/kg) during 5% oxygen breathing reduced mean aortic blood pressure and total peripheral vascular resistance, and increased cardiac output and heart rate, but did not affect left ventricular dP/dt, dP/dt/P, and end-diastolic pressure. Simultaneously, renal and myocardial blood flows increased and myocardial oxygen extraction decreased, while myocardial oxygen consumption did not change significantly. These results suggest that the renin-angiotensin system plays an important role in the hemodynamic responses to severe hypoxia. It appears that angiotensin not only exerts a direct vasoconstrictor action, especially upon the coronary and renal circulations, but also potentiates the cardiovascular effects of sympathetic stimulation that occur during severe hypoxia.
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PMID:Renin-angiotensin system inhibition in conscious dogs during acute hypoxemia. Effects on systemic hemodynamics, regional blood flows, and tissue metabolism. 71 60

Aspirin has been shown to acutely block the natriuretic effect of spironolactone in the mineralocorticoid-treated normal rat, dog, and man. It has been suggested that aspirin is contraindicated in hypertensive patients receiving spironolactone. Five patients with low-renin essential hypertension and two with hypertension due to primary aldosteronism, all of whom have normalized their blood pressure on chronic spironolactone therapy, were cotreated in a double-blind fashion with either aspirin or aspirin-placebo during alternate six-week periods. Aspirin did not appear to alter the effect of spironolactone on blood pressure, serum electrolytes, urea nitrogen, or plasma renin activity.
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PMID:Failure of aspirin to antagonize the antihypertensive effect of spironolactone in low-renin hypertension. 78 8

1. A group of patients with essential hypertension was divided into three categories on the basis of the plasma renin activity. 2. There was no correlation between the plasma renin activity categorized as high, normal or low and the duration of hypertension, the incidence of left ventricular enlargement, the blood urea nitrogen, serum creatinine, cholesterol or uric acid respectively. 3. Analysis of data showed that the incidence of cardiovascular events in the hypertensive population correlated with the plasma renin activity only in combination with known risk factors.
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PMID:Plasma renin activity and cardiovascular disease. 107 64

The influence of a mixture of pig pepsin with renin (in a ratio of 1:1), used instead of renin in making natural cheeses according to the method proposed by the authors, on the content of some products secondary to decomposition of lactic protein and fat because of a dissimilar nutritional value of the latter, was studied. It has been found that cheeses prepared by using the above mixture do not differ from the control ones in the content of soluble forms of nitrogen, essential amino acids, volatile fatty acids, the sum-total of higher fatty acids and differ but slightly (except for butanone-2) in the proportion of various carbonyl compounds. Hence, an inference is drawn on the suitability of using the renin and pig pepsin mixture in making cheeses according to the method proposed by the authors, since the composition and the quantitative content of products secondary to decompesition of lactic protein and fat in test specimens of the cheese did not differ from the control ones which, in turn, points to the identity of the nutritional value of the finished products in either of these cases.
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PMID:[Comparative characteristics of some products of decomposition of lactic protein and fat in cheeses produced with addition of boar pepsin]. 110 40


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