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 results of estimation of renal prostaglandin (PG) excretion showed a significantly decreased excretion of PGE2 by 71% and that of PGF2 alpha--by 28% in rats with hereditary diabetes insipidus (DI), compared to the control Long Evans (LE) rats. The results suggested an inhibition of renal PG synthesis in DI rats due to the absence of stimulatory effect of ADN in DI rats lacking ADH. An inverse correlation between plasma renin activity and renal PG excretion was found (r = --0.36). The renal kallikrein excretion of DI rats was not significantly different compared to that of LE rats. An attempt for explanation of these results was made.
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PMID:The renal prostaglandin kallikrein-kinin-system in Brattleboro rats with hereditary hypothalamic diabetes insipidus. 386 75

The effects of intracerebroventricular (IVT) infusion of angiotensin II (ANG II), the converting enzyme inhibitor SQ 20881, and dopamine were studied in 15 conscious Na-depleted sheep. IVT ANG II (25 ng/min) significantly increased plasma aldosterone (163 +/- 24%) and vasopressin (ADH) (533 +/- 100%). Plasma renin activity (PRA) was decreased to 64 +/- 10% of basal. IVT SQ (1 microgram/min) decreased aldosterone to 70 +/- 10% and ADH to 55 +/- 9% of basal. PRA increased to 124 +/- 10%. There were no significant changes in plasma Na, K, or cortisol levels nor in mean arterial or intracranial pressure after either infusion. Increasing the dose of SQ to 10 micrograms/min resulted in an increased magnitude of change in the same variables. IVT SQ (1 microgram/min) significantly decreased aldosterone level in five nephrectomized sheep. The responses to IVT dopamine (20 micrograms/min) were qualitatively similar to those elicited by IVT SQ. These data support the existence of an endogenous brain renin-angiotensin system (RAS) independent of the renal RAS. ANG II acts centrally to regulate plasma ADH, aldosterone, and PRA levels. The similarity of the responses to SQ and dopamine suggests that a dopaminergic pathway may be involved in these responses.
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PMID:Central effects of angiotensin II and dopamine in sodium-depleted sheep. 388 49

The possibility that the deleterious renal effects of positive end-expiratory pressure (PEEP) might be avoided by prevention of its attendant cardiovascular effects with increasing intravascular volume was investigated in two groups of anesthetized swine. Group 1 (12 swine) were maintained at a normovolemic state and Group 2 (11 swine) were volume expanded with an infusion of lactated Ringer's solution. In normovolemic swine (Group 1), the addition of PEEP to controlled mechanical ventilation (CMV) caused significant decreases in cardiac output and mean aortic pressure. In addition, decreases in urinary output and osmolar, free water, and creatinine clearance occurred. Change from CMV to CMV + PEEP in Group 1 also produced increases in plasma ADH from 4.6 +/- 2.4 to 10.2 +/- 7 pg/ml (P less than 0.01) and renin from 1.8 +/- 1.0 to 4.7 +/- 1.6 ng X ml-1 X h-1 (P less than 0.01), epinephrine from 133 +/- 23 to 1,060 +/- 636 pg/ml (P less than 0.03) and norepinephrine from 46 +/- 15 to 1,427 +/- 839 pg/ml (P less than 0.03). In hydrated swine (Group 2) addition of PEEP to CMV was not accompanied by any significant change in hemodynamic, renal, or hormonal variables. It is concluded that the short-term renal effects of PEEP are mainly due to hormonal responses that are activated by decrease in perfusion pressure. These responses can be obviated by intravascular volume expansion.
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PMID:Renal function during application of positive end-expiratory pressure in swine: effects of hydration. 389 Jun 19

Changes in plasma ADH levels and plasma aldosterone levels (PA) were studied in patients with end-stage renal disease (N = 40). The patients were divided into two groups according to their plasma renin activity (PRA) into a low renin (LR, n = 9) and a high renin group (HR, n = 31). The metabolic clearance rate (MCR) of plasma ADH was also investigated in 4 patients and 5 normal volunteers. Additionally, it was examined whether plasma ADH, aldosterone and renin were permeable through the dialysis membrane. Pre- and post-dialysis plasma ADH levels in LR were similar to those in the HR group. However, pre- and post-dialysis PA in the HR group were significantly greater than those in the LR group. Post-dialysis PRA was significantly increased in HR compared to pre-dialysis, but not in LR. Pre- and post-dialysis plasma osmolality was increased in both groups, but effective plasma osmolality (EPosm) was within the normal range. There was a significant correlation between EPosm and plasma ADH level both before and after haemodialysis, but the majority of the abnormally high values of ADH compared to the normal values was found within the normal range of EPosm. The patients exhibited high blood pressure and a rise in body weight, and haemodialysis caused a significant fall in body weight and blood pressure in both groups. MCR of ADH was significantly lower in the patients than that in normal subjects. Plasma ADH proved to be permeable through the dialysis membrane in all cases, but aldosterone in only a few cases. Renin was not permeable.
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PMID:Effect of haemodialysis on plasma ADH levels, plasma renin activity and plasma aldosterone levels in patients with end-stage renal disease. 390 90

The aging kidney suffers reduction both in mass and in glomerular filtration rate. These changes may be totally or partially due to atherosclerosis and hypertension, which reduce renal blood flow. Superimposed on these processes, and perhaps responsible for primary loss of renal mass irrespective of renal vascular disease, is glomerular damage and involution that is a consequence of adaptive increases in glomerular perfusion pressure that occurs as the number of nephrons decline with age. The data available at this time do not allow us to distinguish between these two potential mechanisms of renal senescence. The decline in GFR is in turn responsible for reduced renal acidification and the reduced renal clearance of drugs that are normally removed by the kidney. Certain renal functions, however, are depressed to a greater extent than is GFR. Both the ability to maximally dilute the urine and to maximally concentrate it are controlled by serum ADH concentrations and by the action of that hormone on the collecting duct. Aged rats do not maximally secrete ADH under conditions of dehydration and the effect of ADH on the kidney is also attenuated. Elderly humans also cannot maximally suppress ADH secretion when serum osmolality is reduced. Likewise, the renin-angiotensin-aldosterone axis is poorly responsive to volume depletion in aging subjects. As a result, elderly individuals cannot maximally retain sodium under conditions of plasma volume contraction out of proportion to reduction in GFR. The kidney is the site of vitamin D1 hydroxylation. Hydroxylation of vitamin D is reduced out of proportion to any reduction in GFR in the rat. There are no data as yet available on the effect of aging and the production of erythropoietin, a principal regulator of red blood cell mass. Neither are there data available on changes that might occur with advancing age in the ability of the aging kidney to metabolize various hormones, such as parathyroid hormone, glucagon, and insulin. The mechanisms and the full biochemical and physiologic consequences of renal senescence remain to be fully elucidated.
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PMID:The aging kidney. 391

HOI induces a significant increase in the cardiac output, which is accompanied by increases in the urinary excretion of water, Na and K. However, the renal responses are not always associated with the cardiac response, suggesting a possible dissociation of two events. Although the urinary excretion of both ADH and aldosterone decreases during HOI, the mechanism for these changes is not clearly understood. The renal responses to HOI, especially the natriuresis, is considerably attenuated in endurance-trained athletes, which may be related to the more moderate inhibition of both ADH and renin-aldosterone systems. The exact role of the cardiac receptors in inducing the renal responses to HOI is still not defined, although the latter receptors are involved in inducing the natriuresis. Finally, important diurnal variations have been demonstrated for the renal responses to HOI, and elucidation of the mechanism for this interesting phenomenon may help understand the overall mechanisms for the development of cardiorenal-endocrine responses to HOI.
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PMID:Cardio-renal responses to a stimulated gravity-free state induced by water immersion. 401 8

The authors, on the basis of the literature and their own studies, envisage the behaviour of the renin-angiotensin system and of ADH during anesthesia. With regard to renin-angiotensin, it would seem that the changes reported in the past are due to the surgical procedure itself or result form haemodynamic changes but that no anesthetic has a direct effect upon the secretion of renin. For ADH, three concepts must be borne in mind: not only is secretion not influenced by anesthetics, but on the contrary anaesthesia decreases the "vasopressin" response to surgical stress. By contrast, the surgical procedure may induce the secretion of ADH responsible for coronary vasoconstriction. Finally, at high doses, ADH would appear to have an inverse antinatriuretic effect resulting in a sodium diuresis.
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PMID:[Antidiuretic hormone, the renin-angiotensin system and anesthesia]. 610 97

MK 421, 25 mg/kg, administered daily by gavage to young spontaneously hypertensive rats (SHRs) from their 4th to 15th weeks of age almost completely inhibited genetic hypertension development. Since heart rate and cardiac index were not drug affected, prevention of genetic hypertension development was solely related to an early, potent and long-lasting limitation of the progressive increase in peripheral resistance which normally develops in SHRs during ageing. MK 421 slightly enhanced vascular responsiveness to exogenous norepinephrine and angiotensin II and reduced myocardial hypertrophy. Plasma renin concentration was increased. MK 421 slightly reduced body growth but did not affect fluid intake, urinary volume and urinary ADH, demonstrating that no water or salt retention developed. Finally, MK 421's preventive effects against genetic hypertension development persisted up to 10 weeks after treatment discontinuation.
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PMID:[Prevention of the development of genetic hypertension by MK 421 in the SHR]. 628 57

We have previously suggested that inhibition of renin release by sodium chloride is related to absorptive chloride transport in the loop of Henle. Infusion of sodium chloride fails to inhibit renin release in the adrenalectomized (Adx) rat, and dexamethasone restores renin responsiveness to sodium chloride. The purpose of the present study was to evaluate the relationship between loop function (urinary diluting and concentration capacity) and plasma renin concentration (PRC) in the Adx rat. After hypotonic sodium chloride infusion, free water clearance (CH2O) of Adx rats (0.56 ml/hr/100 g +/- 0.17 SE) was decreased (p less than 0.01) compared to controls (2.86 ml/hr/100 g +/- 0.29 SE); PRC of Adx rats (61.9 units/ml +/- 11.2 SE) was increased (p less than 0.01) above controls (6.0 units/ml +/- 1.7 SE). These differences persisted after administration of d(CH2)5Tyr(Et)VAVP, a potent ADH antagonist. In separate groups of animals, after water deprivation, urine concentration of Adx rat (1,401 mOsm/kg +/- 45 SE) was less (p less than 0.01) than that of controls (2,117 mOsm/kg +/- 169 SE). Dexamethasone normalized both CH2O and urinary concentrating ability and also decreased PRC in Adx rats. Thus, in the glucocorticoid deficient rat, increased renin release is associated with impaired loop function. The loop defect may account for high PRC that is not suppressed by sodium chloride.
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PMID:Mechanism of increased renin release in the adrenalectomized rat. Adrenal insufficiency and renin. 633 60

The authors have studied on 25 cases of hypercorticism, one of the mechanisms of producing arterial hypertension, the renin-angiotensin system. The study showed that in only 20% of the cases plasma renin activity was high whereas in the remaining 80% other mechanisms were responsible for the hypertension. In the cases in which the plasma activity of renin was high, by studying the changes in the value of electrolytes we were able to derive some understanding of the mechanism of action of the RA2A system. Thus, the literature data show that sometimes the excess of glucocorticoids causes hypertension by activating directly the RA2A system and concomitently inhibiting the renin-kalikrein system (RKKS) and PgS; at other times, the excess of glucocorticoids is exerted on the same renin-angiotensin system, but via ACTH and ADH, the electrolytes values being those that demonstrate the borrowed mechanism.
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PMID:The role of the renin-angiotensin system in arterial hypertension in hypercorticism. 634 18


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