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)

To assess a possible heritability of a disturbed calcium metabolism in relation to blood pressure regulation, 28 young normotensive offspring of either hypertensive or normotensive parents were studied while administered a defined diet with daily sodium chloride of 6 and 20 g/day for 7 days each. Before the high salt diet was begun, the cytosolic calcium concentration ([Ca2+]i) in platelets was elevated in offspring of hypertensive parents, whereas serum electrolytes, plasma renin activity, plasma catecholamines, and 24-hour urinary excretion of sodium and calcium showed no difference between the two groups. On exposure to a high salt diet, the mean blood pressure increased (from 80 +/- 2 to 85 +/- 2 mm Hg, p less than 0.05) in offspring of hypertensive parents. These changes in mean blood pressure were positively correlated with the basal platelet [Ca2+]i (r = 0.61, p less than 0.01), whereas [Ca2+]i did not demonstrate any significant changes. When the subjects were administered the high salt diet, plasma ionized calcium decreased (from 2.37 to 2.21 meq/l, p less than 0.05) and 1,25-dihydroxyvitamin D3 increased (from 32.7 to 40.8 pg/ml, p less than 0.05) with a transient relative hypercalciuria in offspring of hypertensive parents. This increase of 1,25-dihydroxyvitamin D3 was significantly correlated with the changes in mean blood pressure (r = 0.62, p less than 0.01). Disturbed intraplatelet and systemic calcium metabolism may be of predictive value in the development of hypertension.
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PMID:Disturbed calcium metabolism in offspring of hypertensive parents. 159 47

The role of renal alpha 2-adrenoceptors in the regulation of glomerular filtration and renal perfusion is unknown. We studied the effects of alpha 2-adrenergic blockade on renal hemodynamics in six patients with insulin-dependent diabetes mellitus (IDDM) and in six healthy subjects. At the basal state, glomerular filtration rate (GFR) was higher in IDDM although the difference from control levels was not statistically significant. Volume expansion, achieved by infusion of isotonic sodium chloride solution, during placebo infusion induced a significant drop in GFR in healthy subjects but not in IDDM patients. Infusion of the alpha 2-adrenoceptor antagonist idazoxan did not further modify the effect of volume expansion on GFR. Renal plasma and blood flow as well as filtration fraction were not significantly changed by volume expansion or idazoxan infusion. Plasma renin activity and plasma aldosterone levels decreased during volume expansion in both IDDM and control subjects. In conclusion, volume expansion induced decreased GFR in healthy controls but not in IDDM patients. Since infusion of idazoxan did not affect GFR or other parameters of renal hemodynamics, renal alpha 2-adrenoceptors do not seem to be involved in the regulation of renal function. Hence, enhanced renal alpha 2-adrenoceptor activity is not likely to underlie hyperfiltration as seen in IDDM.
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PMID:Effects of alpha 2-adrenergic blockade on renal hemodynamics in patients with insulin dependent diabetes mellitus. 168 5

Small-volume resuscitation with hypertonic saline in combination with dextran appears to be very successful in experimental animals, where better results are achieved than in animals treated with a traditional infusion regime. This effect is apparently related to improved organ blood flow due to reflex vasodilatation. This reflex is based on the arrival of hypertonic solution in the pulmonary circulation. The expansion of intravascular volume would seem to be of secondary importance. Atrial natriuretic peptide (ANP) is released from secretory granules located in atrial cardiocytes. Atrial distention appears to be the predominant stimulus triggering ANP production. In addition to the natriuretic and diuretic effects, ANP leads to vasodilation, especially when vascular tone is elevated; the sympathetic reflex seems to be attenuated. Cyclic Guanosine Monophosphate (cGMP) is an intracellular messenger and is partly released by ANP in the membrane-bound form. Renin excretion is highly influenced by ANP. The object of this study was to evaluate the influence of a hypertonic solution on this hormonal regulatory system. METHOD. This study compared a hypertonic sodium chloride solution (7.5%) in combination with hydroxyethyl starch (6%) (HH) to Ringer's lactate (RL). Six healthy volunteers received 4 ml/kg HH and 1 week later 500 ml RL. The infusion was administered in 20 minutes via a central venous catheter 70 cm in length. Blood pressure, heart rate, hemoglobin (Hb), hematocrit (Hk), colloid osmotic pressure (COP), sodium (Na+), chloride (Cl-), and plasma osmolarity were measured before starting and 5 and 30 min following infusion. At the same times ANP, cGMP, and plasma renin were also determined. RESULTS. Both groups showed no change in blood pressure or heart rate. The decrease of Hb, Hk, and COP in the HH and RL groups indicated the expansion of circulating plasma volume. HH infusion caused significant increases in ANP and cGMP, whereas plasma renin declined significantly. After RL infusion, ANP and renin values were very similar to the HH group except in one volunteer, who showed an extreme increase in ANP (760 pg/ml) 5 min after HH infusion. cGMP did not increase significantly in the RL group. On comparison of the two groups, only a significant difference in plasma osmolarity and in sodium and chloride levels was noted. CONCLUSION. We found that hypertonic NaCl (7.5%) with HH was well tolerated. Release of ANP and cGMP after HH infusion in healthy volunteers was not as high as expected, and the vasodilatory effect of hypertonic solutions was not explained by ANP or cGMP release in this investigation.
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PMID:[Plasma levels of atrial natriuretic peptide, cyclic guanosine monophosphate and renin following 7.5% NaCl + 6% hydroxyethyl starch or Ringer's lactate. A comparative study of 6 normal subjects]. 170 29

Renin secretion from renal juxtaglomerular cells is controlled by the intrarenal blood pressure, sodium chloride load of the organism, sympathetic nerve activity, and a number of hormones. The mechanisms by which these parameters exert their effects are not well understood. However, it is reasonable to assume that they act via signal transduction systems, implying the role of second messenger molecules in the control of renin secretion. This article summarizes present knowledge about the cellular mechanisms of renin secretion. Moreover, current concepts about the mechanisms by which the blood pressure and the sodium chloride load could influence renin secretion are discussed.
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PMID:Molecular mechanisms of renin release. 170 19

Previous physiological and biochemical studies suggest the existence of an endogenous renin-angiotensin system (RAS) in the kidney. However, these data cannot exclude the contribution of the circulating RAS. Proof of the local synthesis of RAS components in the kidney has been obtained recently through the use of molecular biological techniques. Using Northern blot analysis, we have demonstrated the intrarenal expression of renin, angiotensinogen, and angiotensin-converting enzyme messenger RNAs. Employing in situ hybridization histochemistry, we have localized the intrarenal tissue sites of renin and angiotensinogen messenger RNA synthesis. Renin gene expression was found in cells of the juxtaglomerular apparatus. Angiotensinogen mRNA was primarily produced in the proximal convoluted tubule with lesser amounts in glomerular tufts and vasculature. These findings led us to hypothesize that the proximal tubule is a major site of renal Ang II synthesis and that locally synthesized Ang II might directly modulate tubular function. Both genes are subject to feedback regulation. Our studies showed that Ang II exerted a stimulatory effect on angiotensinogen but a negative feedback effect on renin gene expression. Dietary NaCl restriction stimulated the expression of both genes, although the onset of renin gene activation required more prolonged sodium chloride restriction. Furthermore, our data indicated that the sodium cation, irrespective of the anion, was primarily important in regulating renal angiotensinogen mRNA levels. Our studies also showed altered intrarenal renin or angiotensinogen expressions in pathophysiological states, e.g. in experimental heart failure and the spontaneously hypertensive rat. Taken together, these data support the existence of a intrarenal RAS and suggest its potential roles in the regulation of renal function in health and disease.
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PMID:Evolving concepts of the intrarenal renin-angiotensin system in health and disease: contributions of molecular biology. 170 1

Data on the influence of antihypertensive drug treatment on mortality of hypertensive rats are reviewed. Dihydropyridine calcium antagonists, verapamil, the angiotensin-converting enzyme (ACE) inhibitor captopril, and a triple combination of reserpine, hydralazine, and chlorothiazide normalized or markedly prolonged survival. Captopril was less effective in sodium chloride-induced, low-renin Dahl rat hypertension. Dihydralazine prolonged but did not nearly normalize survival. The K(+)-channel activator minoxidil was relatively ineffective. Data on diuretics or beta-blockers are insufficient or unavailable. Calcium antagonists nitrendipine and nimodipine and the ACE inhibitor captopril improved survival and prevented vascular lesions and calcinosis even at doses that failed to achieve normotension. All drugs that normalized survival also reduced heart weights. Minoxidil invariably increased heart weights and failed to improve survival. (Di)hydralazine assumed an intermediate position.
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PMID:Effects of different antihypertensive drug classes on survival in animal models. 171 94

Several studies support the premise that there is a strong relation between obesity and high blood pressure. Although the mechanism for obesity-related hypertension has not yet been fully elucidated, recent studies have suggested that abnormalities in renal sodium handling may be involved in the pathogenesis of obesity-induced hypertension. The purpose of the present study was to determine the effects of an acute saline load on renal excretory function in dogs with obesity-induced hypertension and in normotensive lean dogs. Experiments were performed in two groups of conscious, chronically instrumented dogs. One group of dogs (obese) was fed a high-fat diet for 5-6 weeks, and the other group (lean) ate a normal diet. The body weight of the obese dog group (26.3 +/- 0.7 kg) was 45% higher than the lean dog group (18.1 +/- 0.3 kg). Mean arterial pressure averaged 126 +/- 2 mm Hg in the obese dogs and 100 +/- 1 mm Hg in the lean dogs. The lean dogs had an average heart rate of 104 +/- 7 beats per minute, whereas the obese dogs averaged 134 +/- 8 beats per minute. Plasma renin activity was also significantly higher in the obese dogs. Both groups of dogs were given 135 meq sodium chloride over 60 minutes via an intravenous infusion of isotonic saline. Sodium and water excretion increased significantly in response to the acute saline load. However, the natriuresis and diuresis was markedly attenuated in the obese hypertensive dogs. During the first 40 minutes of saline loading, the increase in sodium and water excretion was 50-70% lower in the obese hypertensive dogs. The results of the present study indicate that obese hypertensive dogs have a reduced capability to excrete an acute sodium load. This abnormality in renal sodium handling may play a role in the pathogenesis of obesity-induced hypertension.
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PMID:Blunted natriuretic response to an acute sodium load in obese hypertensive dogs. 173 Apr 62

Acute renal failure (ARF), an abrupt decline in renal function in its simplest terms, continues to elude precise pathophysiologic definition in human as well as experimental models. In the setting of ischemic or toxic renal injury, the role of sodium chloride as the major constituent of extracellular fluid volume (ECFV) is critically important in the maintenance of renal blood flow. Renal perfusion can be severely curtailed in states of ECFV depletion by activation of the renin-angiotensin axis leading to profound intrarenal hemodynamic alterations. This review will discuss evidence for the role of sodium chloride in the pathogenesis and modification of ischemic and toxic ARF. Much of the data arises from studies in experimental animal models of human disease. The results of clinical studies will be emphasized when available.
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PMID:Role of the sodium ion in acute renal failure. 175 24

Changes in activity of sympathetic-adrenal and + renin-angiotensin-aldosterone systems (SAS and RAAS), hemodynamics and electrolyte metabolism when correcting sodium balance in consideration of their "salt sensitivity" were studied in 83 hypertension stage I and II patients. In moderate restriction of sodium chloride response of the patients was not uniform. "Salt--sensitive" subjects responded positively with improvement of central and peripheral hemodynamics, electrolyte balance in enhanced activity of SAS and RAAS. In salt nonresponders and in paradoxical sensitivity SAS and RAAS show activation, most distinct in paradoxical sensitivity, and worse central and peripheral hemodynamics, electrolyte imbalance.
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PMID:[Various neurohumoral aspects of hemodynamic changes in patients with hypertension after correction of electrolyte disorders]. 176 49

Findings from hypertension research indicate that dietary sodium chloride (NaCl), Na+, and Cl- independently influence blood pressure, electrolyte metabolism, and hormone secretion. In this context, we examined the effects of NaCl, Na+, and Cl- depletion, respectively, on the development of saline preference (salt appetite) in rats. Male Wistar rats were given a normal diet (1% NaCl) for 15 days and tested for salt appetite using a two-bottle choice test, one bottle containing water and the other 0.3 M saline. The animals were then divided into three groups (n = 11/group): one group received low NaCl, another received a Na(+)-deficient, normal-Cl-diet (low Na+), and a third received a Cl(-)-deficient, normal-Na+ diet (low Cl-). Salt appetite was again tested after 19 days on these diets. Both NaCl and Na+ depletion stimulated saline intake (P less than 0.01), whereas salt appetite did not change in the low-Cl- group. Water intake was not influenced by the regimens. In addition, no alterations were noted for weight, systolic blood pressure, plasma Na+ concentration, or blood pH. Dietary Cl-depletion, however, significantly reduced plasma Cl- concentration (P less than 0.05), and reduced plasma potassium in relation to rats depleted in Na+ (P less than 0.05). Plasma renin activity and urinary aldosterone were elevated in low-NaCl and Na(+)-depleted rats relative to the Cl(-)-depleted group (P less than 0.05). These results suggest that salt appetite is increased by dietary Na+ deficiency but not by Cl- deficiency. Salt appetite may be controlled by central or peripheral systems specifically sensitive to Na+ or by hormonal changes characteristic of Na+ depletion, such as the activation of renin and aldosterone observed in the low-NaCl and low-Na+ groups.
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PMID:Selective effects of sodium and chloride depletion on salt appetite in rats. 188 49


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