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)

A double-blind, placebo-controlled parallel study was conducted on the effect of a high daily oral calcium supplementation of 1 g elemental calcium, given twice daily for 16 weeks in normal male subjects, on plasma renin, aldosterone, kallikrein, cGMP, cAMP and calciotropic hormones, intracellular calcium concentrations and plasma total and ionized calcium. After a 1-month run-in period on a limited use of dairy products, the subjects (n = 32) were allocated to a placebo or a calcium group. Placebo or 1 g elemental calcium was administered twice daily in the morning and evening for 16 weeks. All subjects were investigated at baseline and after 1, 2, 4, 8 and 16 weeks of placebo or calcium administration. A decreased intraerythrocyte and intraplatelet Ca2+ concentration was observed in the calcium-treated subjects. Compared with the placebo group, an increase in the plasma renin activity (PRA) in the calcium group was observed after 4, 8 and 16 weeks of oral calcium administration. However, plasma aldosterone and urinary excretion of aldosterone, kallikrein, cGMP and cAMP were not changed during calcium administration. Oral calcium supplementation in these men was also accompanied by a reduction in the plasma concentration of intact parathyroid hormone and 1,25-dihydroxyvitamin D3, an increase in 24-h urinary calcium excretion but no change in the plasma total Ca2+ concentration, serum ionized Ca2+ level and plasma phosphate or 25-hydroxyvitamin D3. Lacidipine tended to increase PRA in the placebo-treated subjects and to decrease it in the calcium-treated subjects: this difference in lacidipine effect between the placebo and calcium group was significant (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of oral calcium supplementation on intracellular calcium and plasma renin in men. 759 37

This investigation focuses on the hormonal response to electrolyte changes and water loss in patients suffering from heat exhaustion, hospitalized in Muna during Hajj seasons. The concentrations of cortisol, aldosterone, renin (PRA), vasopressin (ADH) parathyroid hormone (PTH), adrenocorticotrophic hormone (ACTH) and growth hormone (GH) were determined in venous blood samples drawn from the patients upon admission, during, and after treatment. Highly elevated PRA mean values (396.77 +/- 88.58-462.18 +/- 106.95 ng.ml-1.h-1) were recorded, with no statistically significant difference between the readings. A similar trend was seen for cortisol (42.92 +/- 4.30-60.20 +/- 11.90 ug/dl). Vasopressin (ADH) showed a highly elevated value upon admission (42.48 +/- 18.82 pg/ml), which decreased to 23.66 +/- 8.27 pg/ml during treatment, and declined further to 7.67, ranging between 4.04 and 11.30 pg/ml, thereafter. Statistically speaking, however, there was no significant difference between these readings. PTH concentration, on the other hand, increased from an initial value of 143.31 +/- 47.64 to 245.90 +/- 107.34 pmol/l after treatment, but again there was no significant difference between the values. ACTH concentrations showed no detectable values throughout this study. The GH concentration was within normal throughout, ranging from 4.42 +/- 0.87 to 5.19 +/- 1.78 ng/ml. Aldosterone concentration was significantly reduced in the patients upon admission, with an initial value of 187.93 +/- 21.41 pg/ml (p < 0.05 as compared to normal mean value). During and after treatment, aldosterone values were still significantly lower than normal mean (152.63 +/- 13.47, p < 0.05; 145.2 +/- 17.55, p < 0.01, respectively), thereby shedding some light on the possible etiology of persistent metabolic acidosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Physiological studies on heat exhaustion victims among Mecca pilgrims. 764 64

1. The effects of locally applied parathyroid hormone-related protein (PTHRP), a putative autocrine/paracrine hormone, on vascular diameters and glomerular blood flow (GBF) in the split hydronephrotic rat kidney were studied. As PTHRP interacts with parathyroid hormone (PTH) receptors in all tissues tested so far, the effects of PTHRP were compared with those of PTH. 2. Preglomerular vessels dilated in a concentration- and time-dependent manner that was almost identical for PTH and PTHRP. A significant preglomerular vasodilation (5-17%) occurred at a threshold concentration of 10(-10) mol l-1 PTH or PTHRP, which raised GBF by 20 +/- 2 and 31 +/- 4%, respectively (means +/- S.E.M., n = 6). PTH or PTHRP (10(-7) mol l-1) increased preglomerular diameters (11-36%) and GBF (60 +/- 10 and 70 +/- 8%, respectively) to near maximum. The most prominent dilatation was located at the interlobular artery and at the proximal afferent arteriole. 3. Efferent arterioles were not affected by either PTH or PTHRP. 4. Estimated concentrations of half-maximal response (EC50) for preglomerular vasodilatation and GBF increase were in the nanomolar to subnanomolar range. 5. After inhibition of angiotensin I-converting enzyme by 2 x 10(-6) mol kg-1 quinapril I.V. (n = 6), 10(-8) mol l-1 PTHRP dilated preglomerular vessels and efferent arterioles (9 +/- 1% proximal and 6 +/- 1% distal). 6. We conclude that the renal vasculature of the hydronephrotic kidney is highly sensitive to vasodilatation by PTH and PTHRP, which, in addition, may constrict efferent arterioles by stimulating renin release.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vascular effects of parathyroid hormone and parathyroid hormone-related protein in the split hydronephrotic rat kidney. 765 Jun 15

Pregnancy induced hypertension (PIH) is a common complication in pregnancy and prenatal stage. Because the direct and indirect relationship between low calcium intake and many diseases, such as rachitis, young age myopia and hypertension, calcium supplementation has been a hot topic among nutritionists. Randomized trials of calcium supplementation during pregnancy were conducted in 212 healthy primipara. They were divided into 4 groups and gave 120mg, 240mg, 1g or 2g of calcium daily from 20 to 28 wks of gestation up to delivery respectively. As a result, the incidence of PIH was 8.9%, 7.5%, 8% and 4% respectively in these groups. The control group (106 pregnant women) who did not receive calcium gave an incidence of 18%. Supplementation of 2g of calcium daily showed significant results in lowering the incidence of PIH (P < 0.05) without any adverse effects. In 1992 calcium supplementation was widely used in antenatal-clinic. 200 cases with intake of 2g calcium were compared with corresponding non-calcium supplementation cases, and the incidence of PIH was 7.5% and 16.5% (P < 0.005) respectively. Mediating parathyroid hormone and renin activity are thought to be the effect of calcium on decreasing the incidence of PIH.
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PMID:Calcium supplementation during pregnancy for reducing pregnancy induced hypertension. 771 43

In recent years growing attention has been directed towards the possible role of calcium in the development of pregnancy-induced hypertension and preeclampsia. Several studies describe calcium metabolism in normal and hypertensive pregnancy, but so far, they have shown discrepant and inconsistent results. Intracellular free calcium, which plays an important role in vascular smooth muscle contraction, has been claimed as a pathogenic factor in hypertensive disorders of pregnancy. Although there is discordance in the data, a possible role of intracellular calcium in the development of hypertensive disorders of pregnancy cannot be excluded. Observational studies in pregnant women suggest an inverse association between calcium intake and the incidence of hypertensive disorders of pregnancy. Despite large methodological differences, the results from the calcium supplementation trials support this finding. Although it is rather difficult to isolate the effect of calcium intake from the intake of other mineral elements, results from calcium supplementation trials are supportive for calcium being the most important. Proposed mechanisms by which calcium supplementation may lower blood pressure involve changes in parathyroid hormone (PTH) level, the renin-angiotensin system and calcium as a modifier of vascular agent regulation, but none of these have yet been elucidated. At present, circumstantial evidence suggest a positive role for calcium in the prevention of hypertensive disorders of pregnancy, but definite evidence is lacking and further research is warranted.
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PMID:Calcium metabolism, calcium supplementation and hypertensive disorders of pregnancy. 778 61

There is no doubt that calcium antagonists are effective antihypertensive agents. Their antihypertensive potency is comparable with that of beta-blockers and angiotensin-converting enzyme inhibitors. Blood pressure decreases are dose dependent with no orthostatic reactions, and are more pronounced in patients with lower renin levels, which is demonstrable in both white and black patients; whether the blood pressure response is stronger in elderly patients remains to be ascertained. Blood pressure rises during stress are moderately decreased. Basic documentation has been obtained for first-generation calcium antagonists, and the newer members of this class of drugs--nearly all dihydropyridine derivatives--were developed to achieve greater vascular specificity and a longer duration of action. With calcium antagonists, blood pressure decreases are due to decreases in peripheral resistance. However, blood flow increases do not necessarily persist over time, thus raising the question of what is the mechanism for the long-term decreases in blood pressure. Several studies have shown that blood pressure variability is unchanged with calcium antagonists. However, blood pressure decreases are accompanied by regression of left ventricular hypertrophy, which is understandable in light of the strong correlation between parathyroid hormone and left ventricular hypertrophy. The use of calcium antagonists in the treatment of clinical hypertension can be guided by the following facts: 1) They are metabolically neutral and are accompanied by few or no life-threatening side effects that, when they do occur, tend to disappear over time; 2) They increase blood flow to muscle and help control angina pectoris as well as vasospastic diseases.
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PMID:Antihypertensive effects of calcium antagonists. Clinical facts and modulating factors. 794 73

In societies with several ethnic groups the prevalence of hypertension is abnormally high in black subjects. In addition, blacks are more susceptible to the consequence of high BP. Compared with whites plasma renin is low in blacks independently of age, the level of BP and dietary sodium consumption. No abnormal mineralocorticoid level has ever been consistently reported in blacks to account for their low renin. However potassium intake, prostaglandin and kallikrein excretions are low in blacks and black/white differences exist in the distribution of the restriction fragment length polymorphism at the gene loci for renin. It is hypothesised that the low renin and the propensity of blacks to hypertension result from elevated free cytosolic calcium. Indeed several factors inducing or associated with an increased cytosolic calcium cluster in blacks, e.g. sodium pump inhibition, high intracellular sodium concentration, low plasma ionised calcium, high parathyroid hormone. Furthermore, intensive calcium mobilisation from intracellular stores in response to circulating serum agonists as observed in skin fibroblasts of blacks might be contributive should it occur in all cells including vascular smooth muscle and juxtaglomerular cells.
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PMID:Differences between black and white persons in blood pressure and related biological variables. 800 15

Proteolytic enzymes, lipase, kinins, and other active peptides liberated from the inflamed pancreas convert inflammation of the pancreas, a single-organ disease of the retroperitoneum, to a multisystem disease. Adult respiratory distress syndrome, in addition to being secondary to microvascular thrombosis, may be the result of active phospholipase A (lecithinase), which digests lecithin, a major component of surfactant. Myocardial depression and shock are suspected to be secondary to vasoactive peptides and a myocardial depressant factor. Coagulation abnormalities may range from scattered intravascular thrombosis to severe disseminated intravascular coagulation. Acute renal failure has been explained on the basis of hypovolemia and hypotension. The renin-angiotensin alterations in acute pancreatitis (AP) as mediators of renal failure need to be studied. Metabolic complications include hypocalcemia, hyperlipemia, hyperglycemia, hypoglycemia, and diabetic ketoacidosis, of which hypocalcemia has been long recognized as an indicator of poor prognosis. The pathogenesis of hypocalcemia is multifactorial and includes calcium-soap formation, hormonal imbalances (e.g., parathyroid hormone, calcitonin, glucagon), binding of calcium by free fatty acid-albumin complexes, and intracellular translocation of calcium. Subcutaneous fat necrosis, arthritis, and Purtscher's retinopathy are rare. The various prognostic criteria of AP and other associated laboratory abnormalities are manifestations of systemic effects. Early recognition and appropriated management of these complications have resulted in improved prognosis of severe AP.
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PMID:Acute pancreatitis: a multisystem disease. 804 85

Using a muscle bath technique the vascular response to KCl, noradrenaline, angiotensin II, acetylcholine, and sodium nitroprusside were evaluated in 13 patients with diabetes mellitus (DM group) and 15 nondiabetic (non-DM group) chronic renal failure patients treated with haemodialysis. There were no differences in age, duration of haemodialysis, blood pressure and the levels of plasma renin activity, noradrenaline, and parathyroid hormone between groups. After informed consent was obtained, a small piece of forearm vein was resected during the blood access surgery. The ring preparation of the blood vessel was sustained in the muscle bath filled with Krebs-Henseleit solution and the isometric tension development was recorded. All drugs produced concentration dependent responses in the ring preparations of both groups. Although there were no significant differences in Emax values for KCl- and angiotensin-II-induced contractions between groups, the value for noradrenaline in the DM group was significantly less than that in the non-DM group. Sodium nitroprusside completely relaxed the ring preparation precontracted by 10(-5) M noradrenaline. However, the response to acetylcholine in the DM group was significantly weaker than that in the non-DM group. These results suggest a reduced vascular response to noradrenaline and acetylcholine in dialysed diabetic renal failure patients, which may relate to the autonomic nervous system dysfunction.
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PMID:Vascular response to vasoactive agents in dialysed patients with chronic renal failure with and without diabetes mellitus. 817 67

The changes in blood volume (BV), atrial natriuretic peptide (ANP), plasma renin activity (PRA), aldosterone (Aldo), norepinephrine (NE), epinephrine (Epi), parathyroid hormone (PTH), arginine vasopressin (AVP) and the cyclic nucleotides cAMP and cGMP were measured during a fluctuating BV cycle in 15 patients with end-stage renal failure maintained on chronic hemodialysis (HD). HD consisted of 4 periods of about 60 min each. The first half of each HD period consisted of ultrafiltration (UF) greater than 1,000 ml/h, and the second half consisted of no UF. Changes in relative BV were measured using continuous hemoglobinometry. Total BV at the end of treatment was 74.3 +/- 6.9% of the pretreatment volume. A significant positive correlation between BV and the levels of ANP, PTH, Epi and cGMP and an inverse correlation between BV and PRA, Aldo, AVP and NE were demonstrated. While mean values of NE and AVP levels were directly related to actual changes in BV, individual values did not homogeneously reflect this relationship. The cyclic nucleotides cGMP and cAMP did not follow immediate BV changes, but showed a significant decrease correlated with diminished BV. Based on a pre-postdialysis analysis, significant changes in PRA and Aldo were missing. It seems possible that vascular stability in dialysis patients may be maintained by the response of NE and AVP, and not by the renin-aldosterone system. The changes in ANP and cGMP values correlated most significantly (r = 0.38 and r = 0.51, p < 0.005) with the changes in BV, but no single variable could explain the blood pressure regulation during HD with intermittent rapid UF.
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PMID:Response of vasoactive substances to intermittent ultrafiltration in normotensive hemodialysis patients. 824 91


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