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 cardiovascular effects of the synthetic amino terminal fragment of parathyroid hormone, PTH(1-34), were studied in intact conscious sheep. Physiological doses of bovine (b) PTH(1-34), 0.188, 0.376, 0.56 and 0.75 micrograms kg-1 h-1 were infused in random order into conscious sheep for periods of 1 h each. Isotonic saline was infused as a control. Mean arterial blood pressure (MABP) decreased from 99.2 +/- 1.2 mmHg during the control infusion to 88.9 +/- 1.4 mmHg during infusion of the highest dose of PTH. Heart rate (HR) increased from 81.6 +/- 7.3 beats min-1 during the control infusion to 142.3 +/- 14.0 beats min-1 at the highest PTH dose and plasma renin activity (PRA) increased from 0.33 +/- 0.15 ng ml-1 h-1 to 1.54 +/- 0.46 ng ml-1 h-1. Cardiac output (CO), calculated by an indirect method, increased to 176 +/- 28% of the control values. The changes in all four parameters were dose dependent. Renal blood flow (RBF) increased during the PTH infusion period.
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PMID:Cardiovascular effects of parathyroid hormone in conscious sheep. 205 28

Several abnormalities of calcium metabolism have been described in patients with essential hypertension, and they have been linked to the pathogenesis of hypertension. Intestinal calcium absorption has been shown to be decreased in rats with spontaneous hypertension, but it has not been studied in patients with essential hypertension. In these studies we have for the first time measured intestinal absorption of calcium (using oral and intravenous administration of 47Ca), along with other parameters of calcium metabolism, in 14 patients with essential hypertension and normal renal function and in 16 normal subjects. There was no difference in serum total or ionized calcium, serum phosphorus, parathyroid hormone (PTH), 25-hydroxyvitamin D (25(OH)D), 1,25-dihydroxyvitamin D (1,25(OH)2D), and 24,25-dihydroxy-vitamin D(24,25(OH)2D) among hypertensives and normotensives. The urinary excretion of calcium, on the other hand, was greater in hypertensive than in normotensive subjects (195 +/- 33 v 107 +/- 13 mg/24 h, P less than .05). There was also no difference in intestinal absorption of calcium after 2 and 24 h among hypertensives and normotensives. When hypertensive patients were stratified according to plasma renin activity (PRA) we found that patients with low PRA had higher intestinal absorption of calcium at 2 h (23 +/- 2.9 v 18 +/- 0.6%, P less than .05) but not at 24 h. Serum total and ionized calcium, PTH, and 1,25(OH)2D were not different between patients with low and those with normal-high PRA. The major derangement of calcium metabolism in patients with essential hypertension is hypercalciuria. This abnormality is more pronounced in patients with low PRA, and it may lead to increased vitamin D-dependent intestinal absorption of calcium.
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PMID:Intestinal absorption of calcium and calcium metabolism in patients with essential hypertension and normal renal function. 206 73

The effects of intravenous calcium infusion on blood pressure (BP) and total peripheral vascular resistance (TPR) were investigated in seven normotensives at rates of 3.75, 7.5 and 15.0 mg/kg per h for 1 h. The infusions increased serum calcium levels, with significant elevations of BP and TPR, but had no effect on cardiac output, indicating that the TPR elevation induced the BP rise. The increase in serum calcium was correlated with elevations of systolic, diastolic and mean BP and TPR (r = 0.74, 0.78, 0.77 and 0.82, respectively; P less than 0.001); greater increases in serum calcium resulted in greater elevations of TPR and BP. The serum calcium increase was also associated with reductions in plasma parathyroid hormone and renin activity, and an increase in plasma aldosterone, which might have contributed to the rise in BP. Our results suggest that an increased serum calcium level led to calcium influx into arterial smooth muscle, which increases cytosolic calcium, induces muscle contraction, and thereby produces arterial vasoconstriction, leading to elevations of TPR and BP.
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PMID:Correlation of increased serum calcium with elevated blood pressure and vascular resistance during calcium infusion in normotensive man. 216 93

Racial differences in the regulation of Na+, K+, and Ca2+ have been shown both at the systemic and cellular levels. These include a higher incidence of "salt sensitivity," lower urinary K+ excretion, lower plasma renin activity, and higher circulating levels of immunoreactive parathyroid hormone and 1.25 dihydroxyvitamin D in blacks than in whites. Blacks exhibit a higher erythrocyte Na+ concentration, coupled with a lower maximal initial reaction velocity of erythrocyte Na,K-ATPase. Blacks also appear to differ from whites in erythrocyte Na+, K+ cotransport and Na-Li countertransport. Moreover, they show a higher activity of the Na(+)-H+ antiport in skin fibroblasts and a greater response of cellular Ca2+ signaling to agonists in serum. Mechanisms linking some of these racial differences in ionic metabolism to the increased propensity of blacks to develop essential hypertension are proposed, and the epidemiology and characteristics of this disease in blacks are reviewed.
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PMID:Essential hypertension in blacks: epidemiology, characteristics, and possible roles of racial differences in sodium, potassium, and calcium regulation. 217 6

There is evidence in the literature that calcium entry blockers are able to affect calcium-dependent hormone secretion and therefore can influence sodium and calcium metabolism. We have studied in 18 mild to moderate hypertensives (27-65 yrs) the effects of chronic treatment with nicardipine, a dihydropyridine derivative, vs placebo on: 1) renin-angiotensin-aldosterone axis; 2) parathyroid hormone and calcium metabolism; 3) daily sodium and calcium urinary excretion. After a 2-week placebo wash-out when any antihypertensive treatment was withdrawn, patients were kept on a well balanced normocaloric diet without salt intake restriction. Blood pressure, plasma renin and serum aldosterone after a 1-hour standardized walk, serum PTH, serum and 24-hour urinary Na, K, Ca, P, Mg were measured. Thereafter patients were randomly and blindly given nicardipine 20 mg tid or placebo tablet tid for 2 months. At the end of this period the same measurements were repeated. Blood pressure significantly dropped during nicardipine (from 165/96 +/- 19/9 vs 150/88 +/- 16/9 mm Hg P less than .05) without change in heart rate. No change was observed on placebo. Plasma renin, serum aldosterone, serum parathyroid hormone and serum and urinary electrolytes did not change during active and placebo treatment. The results of this study suggest that chronic nicardipine does not affect hormone secretion.
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PMID:The effects of nicardipine on sodium and calcium metabolism in hypertensive patients: a chronic study. 217 77

Mild hypercalcaemia associated with primary hyperparathyroidism has been increasingly recognized with the use of automated biochemical screening. Management is often difficult as symptoms are often absent or non-specific. Accordingly, we employed the hypocalcaemic effect of the diphosphonate APD to assess the effect of an acute fall in plasma calcium on indices of general well being, blood pressure, and vasoactive hormones in patients with mild primary hyperparathyroidism. Ten patients were studied in a randomized single blind, placebo-controlled cross-over study, using 30 mg APD intravenously or control saline infusion, over 2 h. Metabolic measurements, formal tests of muscle strength and cognitive function, and a standardized questionnaire were assessed 7 days after infusions. Albumin corrected plasma calcium was significantly lower (mean 2.49 +/- 0.04 SEM mmol/l) after APD when compared to control values (2.70 +/- 0.06 mmol/l, P less than 0.001). Twenty-four-hour urinary calcium, plasma magnesium and absolute monocyte count decreased significantly, whereas plasma parathyroid hormone increased after APD (P less than 0.05). There was no significant change in hypercalcaemic symptoms, muscle strength or cognitive function, and blood pressure, renin, aldosterone and atrial natriuretic peptide did not change. Side-effects, when they occurred, were mild. It is concluded that APD is a safe and effective means of lowering plasma calcium in mild primary hyperparathyroidism, but these acute reductions are associated with little or no improvement in clinical status in these patients.
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PMID:Aminopropylidine diphosphonate (APD) in mild primary hyperparathyroidism: effect on clinical status. 218 63

Although altered cellular calcium handling plays a critical role in the pathophysiology of hypertension, little attention has been focused on the impact of calcium regulating hormones on this process. Recent research provides evidence that parathyroid hormone, calcitonin, 1,25-dihydroxyvitamin D, as well as newly described factors such as calcitonin gene-related peptide (CGRP), exert target-organ-specific actions in cardiac and peripheral vascular tissues, are linked to the renin-aldosterone system, and thus to the control of sodium metabolism, and may directly participate in the hypertensive process, especially in low renin and salt sensitive forms of hypertensive disease. The metabolic set-point of these linked renin and calcium hormone systems, which serve to transduce environmental dietary mineral signals at the cellular level, determines the blood pressure consequences of sodium and calcium loading and/or restriction, and helps to explain the heterogeneous and seemingly inconsistent effects of these dietary maneuvers on blood pressure. Measurement of renin and calcium factors in hypertension thus provides a physiological basis for individualized therapeutic recommendations in human hypertension.
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PMID:Calciotropic hormones in human and experimental hypertension. 222 65

Since 1960 we have diagnosed phaeochromocytoma (paraganglioma) in 10 children. The cases include a 15 year old girl who over a three year period presented with multiple paragangliomata and an associated malignant carotid body tumour. All children were hypertensive, eight of 10 presenting with severe headaches. Diagnosis was based on finding a raised urinary vanillylmandelic acid excretion and plasma noradrenaline concentration. In addition six of eight children were hypercalcaemic with raised plasma calcitonin concentrations; plasma parathyroid hormone concentrations were high in two of seven and four out of eight children had raised plasma renin activities on presentation. No child, however, was found to have a multiple endocrine neoplasia syndrome. Despite the introduction of newer techniques for the detection of catecholamine producing tumours we found that selective arteriography and venous catecholamine sampling were superior for tumour localisation compared with ultrasound scanning, computed tomography, and metaiodo-benzyl-guanidine (MIBG) scanning.
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PMID:Phaeochromocytoma--investigation and management of 10 cases. 233 2

In studying the metabolic effects of diet potassium (K+) variation in normal humans, we noted that varying diet K+ within its normal range influenced inorganic phosphorus (Pi) homeostasis and serum calcitriol (1,25-dihydroxyvitamin D) levels. In six men who ingested a constant whole-foods diet containing (per 70 kg body wt) 27 mmol/day Pi and 52 mEq/day K+, we increased diet K+ to 156 mmol/day with supplements first of potassium bicarbonate (KHCO3) alone and then of potassium chloride (KCL) alone, each for eight days interrupted by an eight-day recovery period of no K+ supplement. Urine Pi decreased promptly with either K(+)-salt, each inducing a persisting retention of 7 to 10 mmoles Pi, which was dumped during recovery. Fasting serum [Pi] increased with either K+ supplement (P = 0.022, repeated measures analysis of variance); the composite mean serum [Pi] for the two K(+)-supplement periods exceeded that for the two periods without supplements (P less than 0.01, paired t-test). Conversely, the concentrations of serum calcitriol decreased with either K+ supplement (P = 0.020). Among subjects, the diet K(+)-induced increases in serum [Pi] correlated with those in plasma [K+] (r = 0.64, P = 0.027); the decreases in serum calcitriol concentration correlated with the increases in serum [Pi] (r = -0.69, P = 0.014). There were no significant differences among periods in serum parathyroid hormone, ionized calcium, urine cyclic AMP excretion, plasma renin activity, body weight, serum albumin, or creatinine clearance; plasma volume decreased slightly during KCL but not during KHCO3 periods.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dietary potassium influences kidney maintenance of serum phosphorus concentration. 234 30

Studies were undertaken to extend previous experiments of the interaction between calcium and parathyroid hormone on renin synthesis by the kidney. Intact normovolemic mongrel dogs between 15 and 25 kg were used for all studies. Plasma renin activity (PRA) was measured by radioimmunoassay. Hypocalcemia produced by thyroparathyroidectomy or chelation with EDTA resulted in an elevated PRA of 3.76 +/- 0.85 ng/ml/h in 17 normotensive dogs compared to 1.52 +/- 0.29 ng/ml/h in 14 normocalcemic normotensive dogs (p less than 0.05). In 5 renovascular dogs, calcium-channel antagonism with nifedipine resulted in a higher PRA of 31.8 +/- 0.5 compared to 11.9 +/- 1.1 ng/ml/h in 23 control renovascular dogs not receiving nifedipine (p less than 0.001). The reactive hyperreninemia following angiotensin blockade was greater in 22 hypocalcemic (10.94 +/- 2.03 ng/ml/h) normotensive dogs compared to 14 normocalcemic normotensive dogs (1.32 +/- 0.34 ng/ml/h, p less than 0.001). Similar results were obtained with angiotensin blockade in nifedipine-treated animals compared to angiotensin blockade in nonnifedipine-treated normotensive dogs. Results with angiotensin blockade on PRA levels in renovascular dogs were found similar to those described with angiotensin blockade in normotensive dogs. We conclude from these studies that calcium reduction, independent of a rise in parathyroid hormone, or calcium-channel blockade was associated with an elevation of PRA in normotensive and renovascular hypertensive dogs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of changes in serum calcium and parathyroid hormone on plasma renin in intact mongrel dogs. 240 56


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