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 estimate the contribution of the specific defect in proximal and distal tubular reabsorption of sodium to renal salt wasting, fractional sodium excretion, distal tubular sodium delivery, and distal tubular sodium reabsorption were determined in 11 healthy premature infants. The study was performed on the seventh day and at weekly intervals thereafter up to the sixth week of life. Sodium clearance and fractional sodium excretion decreased significantly with increasing postnatal age (P less than 0.001). There was no significant alteration in either osmolar or free-water clearances. Distal tubular sodium delivery steadily decreased from 4.96 +/- 0.66 (mean +/- SE) in the first week to 3.3 +/- 0.41 ml/minute/dl GFR in the sixth week of life (P less than 0.05). Distal tubular sodium reabsorption was 69.5 +/- 2.36% in the first week, then rose significantly to reach a value of 83.7 +/- 1.85% in the second week (P less than 0.001) and remained practically unchanged thereafter. It is suggested that the rapid improvement of distal tubular sodium reabsorption in premature infants might result from forced stimulation by the excessively activated renin-angiotensin-aldosterone system.
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PMID:Postnatal development of renal sodium handling in premature infants. 49 Feb 50

The importance of salt and water in the pathophysiology of the hypertensive state is well recognized. The current study is the first to report simultaneous measurements of red blood cell mass, plasma volume, extracellular fluid and total body water levels. Studies were performed in 82 white men, 14 with normal blood pressure and 16 with low renin and 52 with normal renin hypertension. The results indicate that subjects with normal renin hypertension compared with age-matched controls are characterized by an absolute increase (1.5 liter/m2) in intracellular fluid (total body water minus extracellular fluid). Furthermore, the ratio of extracellular fluid to total body water is decreased (0.43 to 0.38). No volume differences were found between subjects with low renin hypertension and age-matched subjects with normal renin hypertension. We conclude that subjects with normal renin hypertension compared with age-matched peers are characterized by an expanded intracellular fluid and that subjects with low renin hypertension do not exhibit a unique volume disorder.
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PMID:Volume studies in men with mild to moderate hypertension. 49 11

Studies of 16 adults with nephrotic edema reveal a spectrum of disease, the extremes of which suggest two different pathophysiologic forms. Patients with the "classic" form--vasoconstriction or hypovolemic nephrosis--have high renin and aldosterone levels that are stimulated rather than suppressed by salt-loading but become lower before steroid diuresis. These patients have minimal lesion disease and, perhaps from diffuse capillary damage, tend to have hypovolemia with renin-induced vasoconstriction. Patients with the second, and heretofore undescribed, form--hypervolemic or overfilling nephrosis--have low renin and aldosterone values that rise normally after sodium depletion. Hypertension, mild renal insufficiency, hypervolemia, and steroid resistance with chronic glomerulonephritis are seen histologically. This form appears volume overloaded from impaired renal sodium excretion. In remission of either type, renin system deviations tend towards normal, but one form does not convert to the other. Renin-sodium profiling may help reveal the two forms and predict steroid responsiveness.
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PMID:Nephrotic syndrome: vasoconstriction and hypervolemic types indicated by renin-sodium profiling. 49 1

Circadian variations of plasma renin activity, plasma dopamine-beta-hydroxylase, and urinary aldosterone excretion were measured in man under conditions of high- and low-sodium intake. Plasma renin activity and urinary aldosterone excretion were maximal at 8 a.m. Plasma DBH shows small, biologically insignificant circadian fluctuations. In three subjects on low-salt diets, the values were lower than those in the same subjects on high-salt diets. Expansion of intravascular volume in supine normal volunteers lowered plasma renin and DBH activity, and also resulted in a significant natriuresis. The decline in DBH activity probably reflects a decrease in its release from autonomic nerve endings and thus demonstrates in man an effect of decreasing autonomic activity.
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PMID:Responses of plasma renin activity and dopamine-beta-hydroxylase to increased intravascular volume. 50 49

Responses to the changes in dietary sodium and posture were investigated in 9 young clinically healthy Japanese males who customarily consumed a larger amount of salt than North Americans or Europeans of mixed white ethnic background. Plasma renin activity (PRA), plasma aldosterone concentration (PAC), and urinary aldosterone excretion rate (AER) differed at each end of 3- to 4-day spans on a "control", a high-salt and a low-salt diet and of furosemide administration. PRA and PAC, also determined during the upright position following the supine blood sampling, increased after only 1 hour of standing in each condition (p less than 0.05 or more). PRA and PAC were well correlated in all 4 conditions, regardless of the posture (r = 0.806, p less than 0.001). There were also highly significant correlations between the "supine" PRA or PAC and the preceding 24-hour AER (r = 0.869, p less than 0.001) for PRA; r = 0.855, p less than 0.001 for PAC). Correlation coefficients between PRA and PAC in 9 individual subjects ranged from 0.823 to 0.987. The estimates of constant and slope of the regression line between PRA and PAC varied from subject to subject. The renin-aldosterone axis in response to changes in dietary sodium and posture must be individually assessed.
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PMID:Individual renin-aldosterone responses of clinically healthy young Japanese men to dietary sodium and posture. 50 29

The kidney has a high capacity to produce a spectrum of different acting prostaglandins (PG). In vivo and in vitro studies have shown that renal formation of PG's, possibly in the vasculature of the cortex represents an essential step in the mechanisms regulating the secretion of renin. PG's formed in the cortex seem to participate also in the control of renal vascular resistance and glomerular filtration rate. PGE2 formed in the medulla modulates the hydroosmotic action of antidiuretic hormone and influences the kidney's capacity for urine concentration. Renal PG formation is reduced by high NaCl intake and enhanced by low NaCl intake and in hypokalemic states. These findings make renal PG's good candidates for participation in the regulation of salt and water balance and in the control of blood pressure. Due to the close connection with the renin angiotensin system, alterations in renal PG formation might be involved in the etiology of high and low renin states. Thus, an impairment in the renal cortical production of vasodilating and renin-stimulating PG's could constitute the common denominator for both the reduced renin secretion and the increased vascular resistance which have been reported to be associated in essential hypertension.
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PMID:Formation and action of prostaglandins in the kidney. 53 77

Experiments were conducted to determine whether suppression of the renin-angiotensin-system and inhibition of the tubuloglomerular feedback response offer protection from acute renal failure, as found in chronically-salt loaded animals. The juxtaglomerular renin activity and tubuloglomerular feedback response were inhibited acutely, by saline expansion, or chronically, by DOCA-treatment with saline drinking fluid or salt diet, by high salt diet alone, or by inducing two-kidney Goldblatt hypertension. The chronic pretreatment procedures depressed juxtaglomerular renin to 16, 7, 13 and 4% of control, respectively, inhibited the feedback response to 53, 37, 56, and 38% of control, respectively, but conferred no benefit in the first hours following a nephrotoxin or ischaemia. In contrast, the acute treatment procedure reduced juxtaglomerular renin activity to only 56% and lowered the feedback response to only 71%, but improved renal function after the nephrotoxin, although not after ischaemia. It is concluded that since severe restrictions of renin activity and tubuloglomerular feedback are not protective, neither is primarily involved in generating the functional restrictions early in acute renal failure. The restoration of renal function by saline expansion accompanied only a modest depression of these two systems and suggests that the beneficial effect may result more from volume expansion or diuresis than from suppression of renal renin or inhibition of tubuloglomerular feedback.
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PMID:The early phase of experimental acute renal failure. V. The influence of suppressing the renin-angiotensin system. 57 64

Biochemical investigations in a boy with a salt losing syndrome revealed a very low secretion of aldosterone which did not rise during salt deprivation, in spite of a normal rise in plasma renin activity. Cortisol secretion was normal - but subsequently decreased, while the corticosterone secretion was high. The patient was studied at the age of 5 weeks, 3 months and also at the age of 8 months. He survived until the age of 18 months on treatment with sodium chloride and DOCA, but did not receive glucocorticoids. At autopsy the adrenal glands were absent, but in fat tissue from the upper renal poles foetal adrenal cortex tissue was found. The histological picture agrees well with other cases which could be designated as "foetal-cortex-only" adrenal hypoplasia. The same histological changes were demonstrated in the boy's brother who died suddenly at the age of 6 weeks. The boy's testes were advanced in maturation to a stage of about ten years: spermatocytes and Leydig cells were present.
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PMID:Familial adrenocortical hypoplasia with early clinical and biochemical signs of mineralocorticoid deficiency (hypoaldosteronism). 57 34

The renal medulla is not often considered an endocrine organ, but recent evidence suggests that this part of the kidney may have important antihypertensive, endocrine functions. The antihypertensive factor(s) of the medulla have been localized to the interstitial cells and characterized as neutral and acidic lipids. The acidic lipids, or protstaglandins, have been the more extensively investigated. Animal and human studies indicate that prostaglandins may influence systemic arterial pressure directly or indirectly by promoting excretion of salt and water. Recent evidence suggests that prostaglandins may be mediators of the renin-angiotensin-aldosterone system, thus influencing blood pressure via this system that plays such a key role in blood pressure control.
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PMID:Renal medulla: an endocrine organ involved in blood pressure regulation. 59 1

We assessed the role of the renin-angiotensin system in the response of the renal circulation to restriction of sodium intake in 38 normal patients. Both saralasin (10 to 30 ng/kg/min), an angiotensin antagonist, and SQ 20881 (30 to 300microgram/kg), a converting enzyme inhibitor, induced a dose-related increase in renal blood flow (xenon 133 washout) only when the resin-angiotension system was activated by restriction of sodium intake to 10 MEq/day. Increasing doses of saralasin (100 to 1,000 ng/kg/min) reduced renal blood flow, presumably due to the angiotensin-like action of this partial agonist. The renal vascular response to SQ 20881 paralleled the endocrine response: An identical threshold dose (30 microgram/kg) increased renal blood flow and reduced plasma angiotensin II concentration, which fell despite a progressive rise of plasma renin activity. Plasma bradykinin concentration did not change in response to SQ 20881, which also blocks kininase II. Both agents also induced a small but consistent and statistically significant reduction in arterial blood pressure, which will be important in assessing the pathogenetic significance of a blood pressure reduction in patients with hypertension. This study indicates that angiotensin mediates the renal vascular response to restriction of salt intake in normal man and provides an approach to assessing the role played by angiotensin in the pathogenesis of functional renal disease.
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PMID:Renal vascular response to interruption of the renin-angiotensin system in normal man. 59 39


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