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 determine the importance of alpha 1-adrenergic receptors in the endocrine responses of fetal lambs to hemorrhage, eight chronically instrumented fetal lambs were bled of 20% of their measured blood volume after pretreatment with prazosin (24.8 +/- 2.1 days' gestation) or inert vehicle (124.2 +/- 2.2 days' gestation) according to a randomized, crossover protocol. Cortisol levels increased threefold with prazosin injection and remained elevated after hemorrhage but did not change with hemorrhage after vehicle infusion. Plasma renin activity was unaffected by the injection of prazosin but increased in both groups after hemorrhage. Vasopressin levels were unchanged in the control group throughout the experiment but increased tenfold with hemorrhage after pretreatment with prazosin. alpha 1-Adrenergic receptor blockade removes adrenergic inhibition of cortisol secretion and changes the hypotensive threshold for the secretion of vasopressin.
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PMID:Endocrine responses of fetal lambs to hemorrhage after alpha 1-adrenergic receptor blockade. 290 72

1. Animal data suggest that opiates, halothane anaesthesia and activation of the sympathetic system stimulates release of atrial natriuretic peptide (ANP). To examine whether this is so in man, venous ANP levels were measured in five patients undergoing elective cholecystectomy. 2. Plasma levels of cortisol, aldosterone, norepinephrine and epinephrine increased 3-6 fold during the study. Cortisol-aldosterone relationships were close in all patients (r = 0.73-0.97), whereas plasma renin activity and aldosterone correlations were strong in only two subjects. 3. Baseline plasma ANP concentrations were within the normal range and were not altered by opiate injection, anaesthesia, or surgery. 4. Unlike experimental animals, man exhibits little or no ANP response to opiates, halothane, or surgical stimulation of the sympathetic nervous system.
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PMID:Effect of opiate, general anaesthesia and surgery on plasma atrial natriuretic peptide levels in man. 296 65

Hydrocortisone and aldosterone concentration was determined in 138 patients with arterial hypertension of adrenal and renal genesis in the blood of the adrenal veins and in the cistern of the vena cava inferior, that of deoxycorticosterone in 50 patients, ACTH in 51 and renin activity in the blood plasma of the renal veins in 21 patients. The concentration of steroid hormones adequately reflected adrenal cortex function facilitating differential diagnosis between renal and adrenal pathology variants. Differential diagnostic analysis on the basis of change in the concentration of steroid hormones was found difficult or impossible if the patients received steroidogenesis changing drugs on day, preceding veno graphic examination of the adrenals.
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PMID:[Hormone levels of the blood of the adrenal veins and inferior vena cava in patients with adrenal and kidney diseases]. 299 98

Fetal adrenocorticotropin (ACTH) and renin secretion are increased by a variety of stimuli and decreased by cortisol negative feedback inhibition. However, the time courses of these interactions are unknown. The present studies were designed to test for rapid feedback negative suppression of ACTH and renin secretion in fetal and adult sheep. In chronically catheterized fetal sheep, ACTH and renin secretion were stimulated by intravenous infusion of sodium nitroprusside, a vasodilator drug. Vehicle or cortisol, infused at rates of 1, 2, or 4 micrograms/min for 2 min before and during the infusion of nitroprusside did not significantly alter the fetal ACTH or renin responses to nitroprusside. In five nonpregnant ewes, chronically prepared with skin loops containing the carotid arteries, nitroprusside (20 micrograms X kg-1 X min-1) was infused beginning 2 min after infusion of vehicle or cortisol (3.5 or 7 micrograms X kg-1 X min-1). Cortisol infusion produced a rising plasma cortisol concentration similar to that after stress but did not alter the magnitude of the ACTH response to nitroprusside. The results indicate that cortisol-induced suppression of ACTH secretion does not occur rapidly in the fetal or adult sheep and that the cortisol-induced suppression of fetal plasma renin activity is a slow process.
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PMID:Absence of fast negative feedback control of ACTH and renin in fetal and adult sheep. 300 21

Previous experiments demonstrated that increases in ovine fetal plasma cortisol concentration to maximal stress levels suppressed fetal plasma renin activity and completely inhibited fetal adrenocorticotropin (ACTH) responses to subsequent stress. This study was designed to quantitate the suppressive action of cortisol on both ACTH and renin. Fetal sheep between 117 and 131 days gestation were surgically prepared with chronically implanted catheters. At least 4 days after surgery, vehicle or cortisol (0.25, 0.5, 1, 2, or 3 micrograms/min) were infused for 5 h. One hour after the end of the vehicle or cortisol infusion, fetal ACTH and renin secretion were stimulated by intravenous infusion of sodium nitroprusside. Cortisol infusions suppressed basal plasma renin activity (caused by suppression of plasma renin concentration) to degrees that were related to the increases in fetal plasma cortisol concentration. After cortisol infusions, renin responses to hypotension were apparently suppressed to degrees not obviously related to the rate of cortisol infusion. Fetal plasma ACTH responses to hypotension were completely suppressed by increases in total and unbound fetal plasma cortisol concentration 1.6 and 1.7 ng/ml, respectively. These results demonstrate a high sensitivity of the fetal hypothalamopituitary unit and renin-angiotensin system to cortisol.
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PMID:Sensitivity of cortisol-induced inhibition of ACTH and renin in fetal sheep. 301 Jul 46

Dexamethasone-suppressible hyperaldosteronism is a rare familial syndrome in which hypokalemia, suppression of plasma renin concentration, and elevated aldosterone secretion are corrected by treatment with glucocorticoids. Regulation of adrenocortical function and body electrolytes was studied in two affected brothers. Both were hypertensive (210/128 and 160/106 mm Hg) with hypokalemia (3.3 and 3.5 mM) and low plasma renin concentrations. Aldosterone was elevated intermittently with levels as high as 45 ng/dl (normal range, 4-16 ng/dl). Cortisol concentrations were normal but were correlated with aldosterone levels (r = 0.9 and 0.7). Concentrations of 11-deoxycorticosterone (19 and 21 ng/dl; normal range, 4-16 ng/dl) and 18-hydroxycortisol (1000 and 950 ng/dl; normal range, 34-150 ng/dl) were elevated, and diurnal changes in both were the same as those seen with aldosterone. Infusion of adrenocorticotropic hormone (ACTH) caused exaggerated increases of aldosterone, 11-deoxycorticosterone, and 18-hydroxycortisol; cortisol response was normal. A 4-week trial of dexamethasone normalized blood pressure and caused a natriuresis, a fall in aldosterone, and a rise in plasma renin. Administration of ACTH after dexamethasone treatment again caused exaggerated increases of aldosterone. Aldosterone did not respond to angiotensin II before dexamethasone therapy (r = 0.01), but it showed a normal response after therapy (r = 0.8, p less than 0.01). Neither administration of dopamine (1 microgram/kg/min) nor long-term therapy with bromocriptine (2.5 mg t.i.d. for 4 weeks) affected aldosterone biosynthesis. Thus, loss of dopaminergic inhibition of mineralocorticoid biosynthesis does not account for hyperaldosteronism in this condition.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dexamethasone-suppressible hyperaldosteronism. Adrenal transition cell hyperplasia? 301 96

The paper is concerned with a study of the effect of an excess of corticosteroids in the body, resulting from single and multiple hydrocortisone administration to rats, on the activity of enzymes involved in the pathway of the renin-angiotensin and kinin systems in different parts of the brain and hypophysis. Hydrocortisone administration to rats resulted in an increase in the activity of the angiotensin converting enzyme in the hypothalamus, hippocamp, striate body and hypophysis, an increase in the renin-like activity in the hypothalamus and hippocamp and its decrease in the striate body. The nature of changes in kininase I activity after the hormone administration was different in the examined parts of the brain. The results obtained indicated that one of the links in the mechanism of corticosteroid action on the renin-angiotensin and kinin system of the brain was the effect of these hormones on the activity of the renin-like, angiotensin converting enzymes and kininase I.
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PMID:[Effect of hydrocortisone on the activity of angiotensin-converting and renin-like enzymes and kininase I in the brain and hypophysis of rats]. 302 May 35

Three male subjects were passively tilted from a supine to a 90 degree head-up standing position on 2 d each at 1 and 31 ATA, then on 1 d of the postdive period. On each day the subjects were tilted once in the morning (0800-1000) and once in the evening (2000-2200). Before each tilt experiment, the subjects were first intravenously cannulated for blood sampling, then assumed the supine position. A blood sample was taken after 10 min in the supine position, and another sample was taken after 15 min of motionless, supported standing. The plasma was analyzed for antidiuretic hormone (ADH), plasma renin activity (PRA), plasma cortisol, and aldosterone. ADH, PRA, and cortisol were significantly increased by tilt, but the responses varied with time of day or atmospheric pressure. Cortisol increased only in the morning tilt (P less than 0.005) and was not affected by pressure. At 1 ATA, PRA was elevated in the morning tilt experiment (P less than 0.005) and not the evening tilt, but the overall response to tilt was greater at 31 ATA than at 1 ATA (P less than 0.005). The ADH response to tilt (P less than 0.025) was unaffected by time of day, but was eliminated at 31 ATA. The basal levels of ADH were also lower at 31 ATA (P less than 0.005). The mechanism of these responses remains unclear, but the eliminated postural stimulation of ADH may account for the eliminated circadian excretory pattern of the hormones. The altered responses to body fluid shifts possibly contribute to the increased aldosterone and decreased ADH frequently observed at hyperbaria.
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PMID:Seadragon VI: a 7-day dry saturation dive at 31 ATA. VI. Hyperbaria enhances renin but eliminates ADH responses to head-up tilt. 331 56

The purpose of this study was to determine whether physiological amounts of cortisol affect the fetal cardiovascular system. Cortisol (4 micrograms/min) or the vehicle was infused intravenously for 5 h into six chronically catheterized sheep fetuses at 127-143 days gestation (term = 145-150 days). In the cortisol-infused animals, plasma cortisol concentration increased from 2.0 +/- 0.6 (SE) to 8.3 +/- 0.9 ng/ml. There was a concomitant decrease in fetal heart rate of 38 beats/min (P less than 1 X 10(-6)) and an increase in arterial pressure. Estimated blood volume decreased by 6% in the cortisol-infused fetuses compared with the vehicle-infused animals (P less than 1 X 10(-4]. In addition, plasma norepinephrine and epinephrine concentrations decreased to 70% of control at the end of the 5-h cortisol infusion, whereas plasma renin concentration decreased to 34% of control. The simultaneous increase in fetal arterial pressure and decrease in estimated blood volume suggest that fetal vascular resistance increased, whereas vascular compliance and/or nonstressed vascular volume decreased. However, this does not appear to be mediated by increases in circulating vasoconstrictor hormone concentrations or increased sympathetic tone. Thus the present study shows that physiological amounts of cortisol have significant effects on the fetal cardiovascular system but the mechanisms are unknown.
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PMID:Fetal heart rate, arterial pressure, and blood volume responses to cortisol infusion. 332 47

The effects of labetalol on the secretion of prostacyclin and plasma-renin activity (PRA) were evaluated, relative to a control group in 24 patients undergoing hip osteotomy. They were randomly assigned to two groups (G-I and G-II) with 12 patients each. Patients allocated to both groups received standard anaesthesia (thiopentone, pancuronium, fentanyl and nitrous oxide). Patients belonging to Group II were given labetalol at a dose of 0.8 mg kg-1. The stable metabolite of PGI2, 6-keto-PGF1 alpha was quantified from urine samples by radioimmunoassay (RIA). Cortisol, PRA and aldosterone were determined from blood samples. A significant increase in 6-keto-PGF1 alpha elimination was observed in G-I. Labetalol administration partially but significantly inhibited this increase. We believe that prostacyclin is involved not through the beta 1 but through the alpha 1 receptors in the secretion of renin.
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PMID:The effect of labetalol on urinary prostacyclin secretion during surgery. 353 90


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