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)

The effects of dietary sodium upon serum and urinary calcium and selected vitamin D metabolites were studied in two groups (n = 10 each) of age and gender matched, white normotensive subjects and patients with normal-renin hypertension. Isocaloric diets were consumed on a metabolic ward with sequential daily sodium intake of 109 meq for 5 days and 9 meq and 259 meq for 6 days each. Values for serum and urinary calcium, phosphorus, magnesium and electrolytes, creatinine clearance, plasma immunoreactive parathyroid hormone, and serum 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D were similar in both study groups on each diet. Measurements of plasma renin activity and serum aldosterone levels were higher in the hypertensive than in the normotensive group on each diet (p less than .05-.01). Serum 1,25-dihydroxyvitamin D and urinary calcium increased on the high sodium diet in the normotensive (p less than .05) and the hypertensive groups (p less than .01). When the data for normotensive subjects and hypertensive patients were pooled by gender, males had a 1 1/2 to 3 times the urinary calcium excretion than females, regardless of diet. The present study indicates that there are no differences in the selected components of calcium and vitamin D metabolism in response to sodium intake in patients with essential hypertension and normal plasma renin activity as compared to normal controls.
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PMID:Normal vitamin D and mineral metabolism in essential hypertension. 305 8

1. Because disturbances of calcium metabolism have been described in hypertension, measurements of plasma and serum concentrations of ionized calcium, total calcium, magnesium and renin were made in 38 patients with essential hypertension and age- and sex-matched control subjects. Urinary excretion of calcium, magnesium and sodium was also determined. 2. The mean serum concentration of ionized calcium was 1.23 +/- 0.04 (SD) mmol/l in the hypertensive group and 1.21 +/- 0.03 mmol/l in controls, and results were similar after correction for pH. There was a weak positive correlation between serum ionized calcium (pH 7.4) and systolic pressure (r = 0.26, P less than 0.02), but no correlation with plasma renin concentration. 3. Although the difference between serum total calcium concentration in the hypertensive (2.29 +/- 0.09 mmol/l) and control (2.26 +/- 0.07 mmol/l) subjects was not significant, there was a significant correlation between total calcium and systolic pressure (r = 0.23, P less than 0.05) which was maintained after correction for other variables. 4. There were no differences in plasma concentrations of parathyroid hormone or 1,25-dihydroxycholecalciferol between hypertensive and control subjects. 5. The hypertensive group showed higher urinary excretion of calcium (5.9 +/- 3.0 mmol/24 h) than controls (4.6 +/- 1.7 mmol/24 h), but the difference was not maintained after correction for sodium excretion. 6. Serum concentrations of magnesium were similar in the two groups, but urinary excretion of magnesium was significantly lower in hypertensive (3.7 +/- 1.3 mmol/24 h) than control (4.5 +/- 1.6 mmol/24 h) subjects and there was an inverse correlation between magnesium excretion and blood pressure (r = 0.3-0.35, P less than 0.01).
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PMID:Calcium and magnesium in essential hypertension. 305 75

The influence of dietary sodium on the antihypertensive effects of verapamil and on components of sodium, water, and calcium metabolism was studied in nine white patients 50 to 65 years old with normal renin hypertension. Diets consisting of 109 and 259 mEq Na were given for 5 days each before the study drug was given. On days 4 and 9, intravenous verapamil (0.075 mg/kg) and oral verapamil (80 mg) were given, followed by 80 mg at 8-hour intervals for three doses. On days 1, 4, 5, 9, and 10, serum and urine electrolytes, osmolality (urine [Uosm], serum [Sosm], and osmolar clearance [Cosm]), calcium plasma renin activity (PRA), and levels of serum aldosterone, 1,25-hydroxyvitamin D, serum ionized calcium, parathyroid hormone, atrial natriuretic hormone (atriopeptin), and erythrocyte calcium and electrolytes were measured. On days 5 and 10, serial plasma samples for measurement of verapamil and norverapamil levels were drawn immediately after the last oral dose of verapamil. After verapamil, Uosm and Cosm decreased during both 109 and 259 mEq sodium diets (Uosm, p less than 0.025; Cosm, p less than 0.01 and p less than 0.025, respectively), but free water clearance increased during each diet (p less than 0.01). Urine volume and sodium excretion increased with the 259 mEq sodium diet (p less than 0.025 and p less than 0.01, respectively). There were no significant changes in measured values of components of calcium metabolism with either diet or after verapamil.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Verapamil-induced natriuretic and diuretic effects: dependency on sodium intake. 316 92

In four-month-old spontaneously hypertensive rats (SHR) the effect of a calcium blocking agent verapamil on blood pressure, ventricular contractility indices, parathyroid hormone (PTH), plasma renin activity (PRA), plasma and adrenal corticosterone content and catecholamines in hypothalamus, myocardium and adrenal gland was evaluated. Calcium and phosphorus in plasma were also determined. Verapamil treatment resulted in a significant decrease in systolic and diastolic blood pressure and a reduction in maximum left ventricular pressure. Verapamil exerted a negative inotropic effect, evaluated by a decrease in dP/dt max and dP/dt neg. PRA was elevated, calcium tended to decrease, and no changes in PTH and phosphorus were found. The hypotensive effect of verapamil in SHR was accompanied by a decrease in plasma and adrenal corticosterone content, and a fall in catecholamine concentration in adrenal glands and myocardium.
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PMID:Effect of calcium blocking agent verapamil on blood pressure, ventricular contractility, parathyroid hormone, calcium and phosphorus in plasma, catecholamines, corticosterone and plasma renin activity in spontaneously hypertensive rats. 328 65

The multisystem involvement in acute pancreatitis (AP) is a reflection of the pancreatic gland's capacity to produce a number of potent vasoactive peptides, hormones, and enzymes. The various prognostic criteria are early evaluations of these metabolic derangements. The pathogenesis of hypocalcemia, long recognized as an indicator of severity of AP, is multifactorial. Imbalances of parathyroid hormone (PTH)-calcitonin, the interactions of glucagon, gastrin and other pancreatic hormones with PTH-calcitonin, the role of free fatty acids in binding serum calcium with albumin, and the translocation of calcium ion in muscles and liver, have been recently described but remain conflicting theories. Yet, the time-honored theory of calcium-soap formation enjoys wide acceptance. Hyperglycemia, hypoglycemia, and occasional ketoacidosis in acute pancreatitis have been studied thoroughly. The complex cause-and-effect relationship between hyperlipidemia with acute pancreatitis needs further study. The coagulation abnormalities seem to be initiated by activated trypsin, and their role in microvascular coagulation appears to form a unifying hypothesis for major organ dysfunction, but this requires further investigation. Adult respiratory distress syndrome may be the result of active enzymes that digest pulmonary surfactant and/or microvascular thrombosis. The depression of cardiac function and shock are suspected to be secondary to vasoactive peptides such as bradykinin, or myocardial depressant factor, whose structure has yet to be elucidated. The renin-angiotensin alterations and renal complications in acute pancreatitis have received scant attention in the literature. The onset of moderate visual disturbances, or even blindness, in a patient with acute pancreatitis as a result of retinal vessel thrombosis is fortunately uncommon. Rare but interesting are the manifestations such as subcutaneous fat necrosis, arthralgia, and pancreatic encephalopathy. Despite the extensive literature on the complexities of the pathogenesis of complications of acute pancreatitis, there have been very few advances in the prevention and management of specific complications. It is hoped that further work on modification of enzymatic disturbances induced in acute pancreatitis will result in its effective treatment and prevention of serious complications.
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PMID:Systemic complications of acute pancreatitis. 328

Total and ionized calcium, parathyroid hormone, calcitonin, and renin activity were measured in 27 untreated patients with essential hypertension. There was no relationship between any of these parameters and diastolic blood pressure. However, a significant inverse relationship was found between diastolic blood pressure and the ratio of either total or ionized calcium to parathyroid hormone (r = -0.40, P less than 0.05; and r = -0.38, P less than 0.05, respectively). The ratios did not correlate with patient age or plasma renin level. This preliminary finding suggests that the role of plasma calcium in hypertension may need to be analyzed in the context of overall calcium metabolism, as influenced by the parathyroid hormone. The role of an altered relationship between plasma calcium level and parathyroid hormone in the pathophysiology of essential hypertension remains to be studied.
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PMID:Parathyroid hormone and calcium. A relationship in hypertension. 341 13

Following a random block experimental design in each case, three repeated measurement studies were carried out in three different groups of conscious rabbits, to investigate the renal effects of increasing doses of intravenous calcium chloride (CaCl2) and bovine parathyroid hormone (PTH). In the first study, each rabbit received either CaCl2 (0.15, 0.3, 0.5 or 1.0 mg kg-1 min-1) or vehicle alone (control) for 160 min. In the second study, rabbits were given either PTH (0.15 microgram kg-1 min-1), CaCl2 (1.0 mg kg-1 min-1), PTH plus CaCl2 (0.15 microgram kg-1 min-1 and 1.0 mg kg-1 min-1, respectively) or vehicle alone; PTH was infused for just over 60 min. In the third study, a much smaller dose (0.05 mg kg-1 min-1) of CaCl2 was infused for 100 min. CaCl2 infusion produced a striking fall in fractional excretion of sodium of at least 50% (P less than 0.01), but this was not dose related, being almost maximal at the smaller doses infused. Although this effect was evident in the absence of any changes in total plasma calcium concentration at the lower doses of CaCl2, renal calcium excretion was increased between 2- and 20-fold (P less than 0.01) at all doses infused. Fractional excretion of chloride doubled at the two higher doses of CaCl2 (P less than 0.01), but potassium excretion was unchanged. There were no consistent alterations in mean arterial blood pressure, effective renal plasma flow, glomerular filtration rate or plasma renin activity (PRA); total plasma calcium concentration was consistently elevated only during infusion of the high dose by just under 1 mmol l-1. PTH infusion had no measured effect on fractional excretion of sodium or renal calcium excretion, but doubled fractional potassium excretion (P less than 0.05). Heart rate and PRA increased (P less than 0.01 and less than 0.05, respectively), the latter by 50%, but systemic pressure and renal haemodynamics were not significantly affected. By contrast, PTH infused with CaCl2 produced a 4-fold rise in fractional sodium excretion and although renal calcium excretion remained increased, it was reduced by ca. 80% when compared with renal calcium excretion during infusion of CaCl2 alone. Infusion of PTH alone increased PRA, but when PTH and CaCl2 were infused together, PRA did not change.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Renal electrolyte excretion and renin release during calcium and parathormone infusions in conscious rabbits. 352 54

Circulating levels of the calcium-regulating hormones, calcitonin, calcitriol, and parathyroid hormone, were analyzed in relation to plasma renin activity in 10 persons with normal blood pressure and in 51 persons with essential hypertension. Calcitriol (p less than 0.008) and parathyroid hormone (p less than 0.01) levels were elevated in hypertensives with low renin activity, whereas calcitonin levels were higher in patients with high renin activity (p less than 0.008), compared with normotensive controls and other hypertensive patients. Continuous relationships were observed between calcitriol levels and plasma renin activity in all patients (r = -0.65, p less than 0.001) and between parathyroid hormone levels and urinary sodium excretion in hypertensive patients with low renin activity (r = -0.63, p less than 0.01). Together, these results support a linkage between calcium metabolism and renin-sodium factors in essential hypertension. Calcium-regulating hormones and the renin-aldosterone system may coordinately mediate the blood pressure effects of differing dietary calcium and sodium intakes at the cellular level by altering cellular handling of monovalent and divalent ions.
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PMID:Calcium-regulating hormones in essential hypertension. Relation to plasma renin activity and sodium metabolism. 353 93

Hypertensive disease is associated with various abnormalities of calcium metabolism although how these abnormalities relate to the elevated pressure remains unclear. Based on the use of renin-sodium profiling, we have defined heterogeneous deviations in circulating levels of ionized calcium and magnesium as well as of the calcium-regulating hormones parathyroid hormone, calcitonin, and 1,25-dihydroxyvitamin D (1,25D), which parallel similar deviations in plasma renin activity. Essential hypertensive subjects with a profile of low renin, lower ionized calcium, and elevated 1,25D respond best to the calcium channel blocker nifedipine, demonstrate an enhanced sensitivity to the blood pressure effects of dietary salt loading, and have significantly lower blood pressures in response to oral calcium supplementation. Hypertensive subjects with the opposite metabolic profile--higher renin activity, higher serum ionized calcium, and lower 1,25D levels--are relatively insensitive to the blood pressure effects of either dietary salt loading or nifedipine, and show no significant hypotensive response to calcium supplements. Altogether, these alterations of calcium ionic and hormonal metabolism suggest that the hormonal control of calcium metabolism is linked to renin system activity as well as to the pathophysiology of the hypertensive process.
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PMID:Calcium metabolism in essential hypertension: relationship to altered renin system activity. 353 39

The factors responsible for the frequent occurrence of hypertension in patients with primary hyperparathyroidism have not been elucidated. Suggested mediators have included hypercalcemia, renal insufficiency, and increased plasma renin activity. However, experimental results have not been reported in any species that test the hypothesis that sustained hypertension in this clinical syndrome is due to consequences of parathyroid hormone (PTH) excess versus unrelated factors (e.g., primary hypersecretion of other hormones, NaCl sensitivity, genetic factors). Moreover, no systematic evaluation of the renin or adrenal cortical responses to chronic PTH excess has been reported in any species. Accordingly, the present studies assessed the effects of chronic (12 days) continuous intravenous b-(1-34) PTH infusion in normal human subjects (n = 4). PTH infusion resulted in persistent hypercalcemia and hypertension, reversible during a 4-8-day recovery period. Transient but significant increases in urinary tetrahydroaldosterone excretion and plasma cortisol concentration were observed as hypercalcemia and hypertension developed. No significant changes in plasma potassium concentration or plasma renin activity were observed, suggesting that hypercalcemia-induced transient hypersecretion of ACTH was responsible for both cortisol and aldosterone responses. The present results suggest that hypertension associated with clinical primary hyperparathyroidism results from either direct or indirect effects of PTH excess, per se, and requires neither the long-term consequences/complications of the clinical disorder (e.g., severe nephrocalcinosis, renal insufficiency) nor primary hypersecretion of additional hormones. These results are consistent with the hypothesis that hypercalcemia alone or in combination with at least permissive levels of PTH can generate short-term, but persistent (12 days) hypertension in human subjects and thus may be the initiating mechanism for hypertension in clinical primary hyperparathyroidism.
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PMID:Chronic continuous PTH infusion results in hypertension in normal subjects. 354 30


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