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)

Young, unilaterally nephrectomized, female Sprague-Dawley rats were given daily sc injections of 19-nor-deoxycorticosterone acetate (19-nor-DOCA) in oil at a dosage of 100 micrograms/day for 21 days and twice that amount for a further 11 days. One group drank distilled water and another drank 1% NaCl solution. Comparable control groups received oil injections. Another group received DOCA at the same steroid dosage and drank saline. Both 19-nor-DOCA-treated groups rapidly became hypertensive and developed cardiac hypertrophy, as did those given DOCA and saline. Saline consumption was greater in rats receiving 19-nor-DOCA, than in those given DOCA. Rats injected with 19-nor-DOCA and given water to drink showed enhanced growth and developed thymus enlargement and displayed hypokalemia and a reduction in both serum renin activity and corticosterone concentration. Plasma sodium concentration was not affected by any form of treatment. Clearly, 19-nor-DOCA is a potent mineralocorticoid and hypertensogenic agent. Since the parent steroid is known to be present abundantly in the urine of rats with regenerating adrenal glands, although circulating amounts have not yet been ascertained in that circumstance, it may be etiologically involved in adrenal regeneration hypertension, which such rats are prone to develop.
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PMID:Influence of 19-nor-deoxycorticosterone on blood pressure, saline consumption, and serum electrolytes, corticosterone, and renin activity. 15 70

This study conducted on the crewmembers of Skylab 3 was designed to evaluate the endocrinological adaption resulting from extend exposure to a space flight environment by identifying changes in hormonal and associated fluid and electrolyte parameters. The three men served as their own controls and were on a constant dietary intake. Complete metabolic collections were performed beginning 21 d before the flight, continuing throughout the flight, for 18 d postflight. Changes in fluid and electrolyte balance have been correlated with weight loss, changes in the excretion of aldosterone, vasopressin, and fluid compartments. Inter-individual variability was demonstrated in most experimental indices measured; however, statistically significant patterns have emerged which include: decreases in body weight and ADH, increases in plasma renin activity, and elevations in urinary catecholamines, aldosterone and cortisol concentrations. Urinary sodium was increased in flight but potassium was only slightly changed. Total body exchangeable K was slightly decreased in all three of the crewmen. Total body water and extracellular fluid were decreased postflight in almost all cases. The measured changes are consistent with the prediction that a relative increase in thoracic blood volume upon transiton to the zero gravity environment is interpretated as a true volume expasion resulting in a net fluid loss. This, in association with other factors, ultimately results in a reduction in intravascular volume leading to an increase in renin and a secondary aldosteronism. Once these compensatory mechanisms are effective in reestablishing positive water balance, the crewemn are considered to be essentially adapted to the space environment. Although the physiological cost of this adaptation must reflect the electrolyte deficit and perhaps other factors, it is assumed that the compensated state is adequate for the demands of the environment; however, this new homeostatic set is not believed to be without physiological cost and could, except with proper precautions, reduce the functional reserve of exposed individuals.
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PMID:Metabolic and endocrine studies: the second manned Skylab mission. 17 19

The role of the renin-angiotensin-aldosterone system in the development of congestive failure has been assessed in the conscious dog by use of the nonapeptide converting enzyme inhibitor. Constriction of the pulmonary artery or thoracic inferior vena cava was maintained for 2 wk while daily measurements were made of plasma renin activity, plasma aldosterone, plasma volume, hematocrit, serum sodium and potassium concentrations, sodium and water balance, body weight, and arterial, caval, and atrial pressures. The initial response to constriction was a reduction in blood pressure, a rise in plasma renin activity, plasma aldosterone, and water intake, and nearly complete sodium retention. In the days after moderate constriction plasma volume and body weight increased (with development of ascites and edema); blood pressure, sodium excretion, plasma renin acvitity, and plasma aldosterone returned to normal. In animals in which blood pressure was not restored, plasma renin activity and plasma aldosterone remained elevated throughout the period of constriction. Single injections of converting enzyme inhibitor reduced blood pressure when plasma renin activity was elevated. Chronic infusion of the inhibitor in dogs with thoracic inferior vena caval constriction prevented the restoration of blood pressure and suppressed the rise in plasma aldosterone; sodium retention and volume expansion were less than in control experiments. Thus the renin-angiotensin-aldosterone system plays an essential role in the maintenance of blood pressure during the genesis of congestive failure. Initially, the restoration of blood pressure is dependent upon circulating angiotensin II; in the later stages, blood pressure is dependent upon the increase in plasma volume.
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PMID:The renin-angiotensin-aldosterone system in congestive failure in conscious dogs. 18 56

The plasma concentrations of cortisol, sodium, potassium and calcium and plasma osmolarity were determined in freshwater silver eels, after intravascular injections of eel renin preparations, mammalian ACTH, mammalian angiotensin II and eel muscle extracts. Arterial blood specimens were taken before and after injection of test substances. Partially purified eel and rat renal renins gave prolonged pressor responses in intact and hypophysectomized eels and in the nephrectomized rat anaesthetized with sodium pentobarbitone. Angiotensin, but not ACTH, produced obvious pressor responses in intact and hypophysectomized eels and in eels without their corpuscles of Stannius. Hypophysectomized eels 4-8 days after operation had reduced plasma cortisol concentrations. No change in cortisol occurred in eels after removal of the corpuscles of Stannius. Eel renin preparations and ACTH gave increased concentrations of plasma cortisol 30 min after injection into hypophysectomized and intact eels. In general, the length of the renin-generated pressor response and the increased cortisol concentration were concomitant occurrences. Angiotensin injected into eels with corpuscles of Stannius removed and into hypophysectomized eels also increased cortisol levels. Control muscle extracts produced no significant changes. There were no acute changes in plasma electrolyte concentrations after the injections. Plasma renin activity measured indirectly by bioassay of angiotensin generated in vitro was more than twice as great in eels adapted to seawater than in eels in fresh water. Plasma renin activity gradually fell when eels were transferred from seawater to fresh water, and increased when the reverse transfer was carried out.
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PMID:Endocrine and environmental influences upon plasma cortisol concentrations and plasma renin activity of the eel, Anguilla anguilla L. 18 Feb 26

The role of the renin--angiotensin system in the regulation of blood pressure in dogs and in human subjects was assessed by the use of the nonapeptide converting enzyme inhibitor (CEI), permitting the following conclusions: 1) In the normal, sodium replete dog, the renin--angiotensin system plays little role in the regulation of blood pressure. 2) As sodium depletion progresses, the renin--angiotensin system becomes increasingly important in the maintenance of blood pressure. In the markedly hypovolemic animal, blocking the conversion of angiotensin I to angiotensin II leads to prolonged hypotension of shock-like levels. 3) The renin--angiotensin system is responsible for the initiation of renovascular hypertension. Blood pressure does not rise during chronic renal artery constriction when the generation of angiotensin II is prevented by the CEI. Although angiotensin II is essential for the initiation of the elevated blood pressure, the renin--angiotensin system plays a decreasing role in the maintenance of the chronic hypertension as sodium and water are retained, and plasma volume increases. 4) In congestive failure induced in the conscious dog by circulatory impairment, the renin--angiotensin--aldosterone system plays an essential role in the compensatory response. During chronic administration of the CEI, the animal cannot compensate even for a relatively mild degree of constriction, and remains hypotensive. In the dog with congestive failure, as in the dog with renovascular hypertension, plasma renin activity (PRA) and plasma aldosterone are elevated early in the syndrome; during this phase, injection of the nonapeptide produces a marked drop in blood pressure. With the retention of sodium and water, and expansion of plasma and extravascular fluid volumes, PRA and plasma aldosterone return to control levels in the new steady state. The inhibitor no longer produces a drop in blood pressure. Thus, the sequential changes in the renin--angiotensin--aldosterone system are remarkably similar in renovascular hypertension and congestive failure. 5) In the normal, salt replete human subject the renin--angiotensin system plays little role in the regulation of blood pressure either in the recumbent or upright posture. However, with relatively mild sodium depletion, the CEI transiently lowers blood pressure even in the recumbent subject. In the absence of angiotensin II such sodium-depleted subjects are unable to compensate when tilted upright, and faint within minutes.
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PMID:Renin--angiotensin antagonists and the regulation of blood pressure. 18 95

Systemic injections of renin that stimulate substantial amounts of drinking in nephrectomized rats can produce plasma renin activities that fall well above the physiological range. Furthermore, increases in plasma renin activities that occur in rats with intact kidneys during experimental hypotension appear to be too low to provide the basis for the observed elevations in water intake. These findings question the contribution of the renin-angiotensin system to thirst under normal physiological conditions.
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PMID:The renin-angiotensin system and thirst: a reevaluation. 18 69

The effects of intrarenal infusion of 1-sar-8-ala angiotension II (P 113) and a converting enzyme inhibitor, SQ 20881, at doses that did not affect systemic blood pressure (2.0 mug/kg per min) were studied in conscious, uninephrectomized dogs. In dogs receiving approximately equal to 5 mEq/day of sodium, intrarenal infusion of P 113 increased renal blood flow (RBF) from 219.8 +/- 32.3 to 282.7 +/- 20.0 ml/min (P less than 0.004), and with intrarenal SQ 20881 infusion from 215.3 +/- 14.2 to 278.0 +/- 22.2 ml/min (p less than 0.005). In sodium-restricted dogs (approximately equal to 5 mEq/day), glomerular filtration rate (GFR) also increased with intrarenal P 113 infusion from 57.9 +/- 5.7 to 66.3 +/- 6.6 ml/min (P less than 0.05), and with SQ 20881 infusion from 43.1 +/- 2.1 to 55.7 +/- 4.5 ml/min (P less than 0.01). Dogs on approximately equal to 5 mEq/day of sodium showed significant increases in plasma renin activity (PRA) with intrarenal infusion of the peptides, unmasking a negative feedback inhibition of renin release by angiotensin II. No increases in RBF, GFR, or PRA were seen with infusion without inhibitors, or in dogs give P 113 or SQ 20881 while on approximately equal to 80 mEq/day of sodium. In addition, angiotensin II inhibition increased sodium excretion during sodium restriction. These findings suggest that intrarenal angiotensin II is intimately involved in renal responses to sodium restriction which result in conservation of sodium and water.
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PMID:Effect of intrarenal angiotensin II blockade on renal function in conscious dogs. 19 Dec 13

One of several factors affecting the secretion of renin by the kidneys is the sympathetic nervous system. The sympathetic input is excitatory and is mediated by beta-adrenergic receptors, which are probably located on the membranes of the juxtaglomerular cells. Stimulation of sympathetic areas in the medulla, midbrain and hypothalamus raises blood pressure and increases renin secretion, whereas stimulation of other parts of the hypothalamus decreases blood pressure and renin output. The centrally active alpha-adrenergic agonist clonidine decreases renin secretion, lowers blood pressure, inhibits ACTH and vasopressin secretion, and increases growth hormone secretion in dogs. The effects on ACTH and growth hormone are abolished by administration of phenoxybenzamine into the third ventricle, whereas the effect on blood pressure is abolished by administration of phenoxybenzamine in the fourth ventricle without any effect on the ACTH and growth hormone responses. Fourth ventricular phenoxybenzamine decreases but does not abolish the inhibitory effect of clonidine on renin secretion. Circulating angiotensin II acts on the brain via the area postrema to raise blood pressure and via the subfornical organ to increase water intake. Its effect on vasopressin secretion is debated. The brain contains a renin-like enzyme, converting enzyme, renin substrate, and angiotensin. There is debate about the nature and physiological significance of the angiotensin II-generating enzyme in the brain, and about the nature of the angiotensin I and angiotensin II that have been reported to be present in the central nervous system. However, injection of angiotensin II into the cerebral ventricles produces drinking, increased secretion of vasopressin and ACTH, and increased blood pressure. The same responses are produced by intraventricular renin. Angiotensin II also facilitates sympathetic discharge in the periphery, and the possibility that it exerts a similar action on the adrenergic neurons in the brain merits investigation.
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PMID:The renin-angiotensin system and the central nervous system. 19 Dec 99

In rats kept under standard conditions urinary aldosterone exretion rate (UAER) and plasma aldosterone concentration (PAC) showed a circadian rhythm with peak values at the beginning of the dark perioith a single dose of DOC (2 mg/kg sc) or given saline as drinking water UAER and PAC decreased to very low levels. Restriction of dietary sodium for 5 weeks increased UAER and PAC 60-fold and 100-fold, respectively. Treatment with ACTH (250 or 500 microng/kg iv) stimulated UAER 8 h following injection and PAC 1 h after injection. In rats treated with a single dose of furosemide (25 mg/kg sc) PAC increased to maximal values within 90 min and reached control values within 24 h. Twenty-four hours-UAER also increased after furosemide treatment. UAER paralleled PAC under all experimental conditions tested. Therefore, our results suggest that UAER is a reliable index of the activity of the renin-angiotensin-aldosterone system in rats under conditions of low and high aldosterone secretion. Measurement of UAER is a useful tool for studies on aldosterone levels in rats over a long period of time.
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PMID:Urinary aldosterone excretion rate and plasma aldosterone concentration in the rat: effect of ACTH, DOC, furosemide and of changes in sodium balance. 19 35

The effects of theophylline ethylenediamine (15 mg/kg i.v.) on plasma renin activity (PRA), diuresis, creatinine clearance and plasma and urinary adenosine 3',5'-monophosphate (cyclic AMP) concentrations were studied in urethane-anaesthetized rabbits with and without pretreatment with indomethacin (5 mg/kg i.v.). Theophylline induced a several-fold increase in urinary sodium and water excretion, raised PRA from 76 +/- 15 TO 239 +/- 83 (S.E.M) ng/ml/h (p less than 0.05) and increased urinary cyclic AMP excretion from 0.21 +/- 0.04 to 0.50 +/- 0.08 nmol/min/kg/kidney (p less than 0.05) without any change in arterial plasma cyclic AMP concentration. The ratio between the clearance of creatinine and cyclic AMP was unchanged. After indomethacin pretreatment the theophylline-induced natriuresis was significantly reduced (p less than 0.05), while the effects of theophylline on PRA and urinary cyclic AMP excretion were unchanged. Under the present experimental conditions, indomethacin reduces renal prostaglandin biosynthesis by over 95%. our results indicate that prostaglandins might be concerned with the natriuretic effects of theophylline but not with the effect on PRA.
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PMID:Effect of indomethacin on the renal actions of theophylline. 19 97


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