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Query: UMLS:C0033036 (APC)
 10,214 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To assess the hypothesis that aldosterone may have direct vasoconstrictive action, the acute effects of canrenoate potassium (Soldactone, S), an aldosterone antagonist, on hemodynamics and hormonal responses were determined before and after the intravenous administration of 2 mg/kg S in 11 patients with primary aldosteronism (PA), 9 patients with essential hypertension (EH), and 5 patients with renovascular hypertension (RVH). S caused a significant -12 +/- 2 mm Hg decrease in MBP in PA, -5 +/- 2 mm Hg in EH, and -4 +/- 1 mm Hg in RVH. Reduction in MBP was significantly higher in PA than in the others and there was a negative correlation between changes in MBP and basal PAC. The cardiac index did not change throughout the study in all groups, which led to a significant reduction in total peripheral resistance index (TPRI) in PA but not in the others. There was a significant correlation between changes in MBP and TPRI (r = 0.82, p less than 0.01). PRA did not change throughout the study, but PAC and cortisol were significantly elevated. There were no correlations between changes in MBP and hormonal responses. In conclusion, S resulted in a significant reduction of MBP mediated by a significant reduction of TPRI. These results suggest that aldosterone may have direct vasoconstrictive action and this extrarenal effect of aldosterone may be involved in the regulation of blood pressure.
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PMID:Extrarenal role of aldosterone in the regulation of blood pressure. 339 Mar 21

A 17-year-old female weighing 37 kg and 140 cm in height was referred to our hospital for evaluation of dwarfism and primary amenorrhea. She was delivered with 3350 g in weight and 50 cm in height after a ten month pregnancy without complications. No abnormal findings were revealed in physical appearance except critomegaly. Episodes of nausea, vomiting and dehydration were rare throughout her childhood, but she had a tendency to salt craving. At the age of 14, her height was 140 cm. On admission, her physical development was markedly retarded for her age, except external genitalia. Diffuse pigmentations on the trunk and extremities were observed. Her blood pressure was normal (112/62 mm Hg). Serum potassium concentration was 2.9 mEq/L. Arterial-blood gas analysis revealed metabolic alkalosis. Both of renin activity (PRA) and aldosterone concentration (PAC) in plasma at rest were markedly elevated to 15.5 ng/ml/h and 107.1 ng/dl, respectively. The plasma concentrations of pregnenolone (1449 ng/dl), progesterone (178 ng/dl), 17-OH-pregnenolone (1613 ng/dl), 17-OH-progesterone (180 ng/dl), dehydroepiandrosterone (3706 ng/dl), androstendione (824.6 ng/dl) and testosterone (900 ng/dl) were high, whereas deoxycorticosterone (15.7 ng/dl), corticosterone (0.65 microgram/dl) and cortisol (6.8 micrograms/dl) were within normal limits. Urinary 17-KS excretion showed high levels between 65.7 and 109.4 mg/day, while urinary 17-OHCS excretion was normal (5.7-7.0 mg/day). Vascular response to angiotensin II (A-II) was attenuated. Distal fractional chloride reabsorption was decreased (CH2O/CH2O+CCl = 0.62, normal: 0.92 +/- 0.04). Moderate hyperplasia of the juxtaglomerular cells was demonstrated in biopsy specimen of the kidney. Cytogenetic studies showed a 46, XX chromosome constitution with translocation of the long arm of chromosome 6 to the short arm of chromosome 9. Her mother as well as younger brother and sister, whose electrolytes and arterial-blood gas analysis showed normal values, had chromosomes with the same translocation. Treatment with dexamethasone (2 mg/day) reduced every adrenal steroids to normal range, but PRA and PAC remained high levels. Furthermore, neither hypokalemic alkalosis nor vasoreactivity to exogenous A-II was improved. Indomethacin (75 mg/day) decreased urinary excretion of prostaglandin E2 from a high level of 738.4 ng/day to 433.4 ng/day and normalized metabolic alkalosis. Vascular response to A-II was moderately improved. However, serum potassium remained low.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A case of 21-hydroxylase deficiency and Bartter's syndrome associated with a balanced 6-9 translocation]. 349 Oct 9

Aldosterone secretion in man is stimulated by potassium, ACTH, and angiotensin II and is inhibited by dopamine (DA). In normal sodium-replete supine individuals, aldosterone secretion is under maximum tonic inhibition by DA. Dopaminergic control of aldosterone secretion is modified by dietary sodium depletion. To determine the physiological significance of dopaminergic inhibition of aldosterone secretion, we studied the effect of DA on the aldosterone response to upright posture. Twelve normal men were studied while eating an ad libitum sodium diet, and the effect of DA was determined in the supine and upright positions. Plasma aldosterone (PAC), plasma cortisol (F), plasma aldosterone-stimulating factor (ASF), PRA, and blood pressure were measured while the men were supine and after 4 h of upright posture during an infusion of 5% dextrose vehicle and during a DA infusion of 4.0 micrograms/kg X min. The men also were studied as a time control in the supine position while receiving vehicle or DA. PAC increased from a mean basal value of 20.4 +/- 3.2 ng/dl (+/- SE) by 25.9 +/- 5.1 ng/dl to a peak of 44.4 +/- 2.4 ng/dl in response to upright posture during vehicle infusion. The PAC response to upright posture was reduced to 7.4 +/- 1.8 ng/dl (P less than 0.05) when DA was infused. The increase in PRA with upright posture was 3.7 +/- 1.3 ng/ml X h during the vehicle infusion and 4.1 +/- 1.1 ng/ml X h (P = NS) during the DA infusion. ASF, F, and blood pressure were not altered by upright posture and DA. PAC did not change in the six men infused with DA while supine. Therefore, DA inhibits upright aldosterone responses without affecting PRA, ASF, or F.
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PMID:Dopamine inhibits the aldosterone response to upright posture. 351 47

CA levels, PRA, PAC responses to low and high sodium dialysates in haemodialysed patients were investigated. Increased levels of dopamine (DA), adrenaline (A) and noradrenaline (NA) were found during dialysis and ultrafiltration with high sodium dialysate (148 mEq/l), and significantly higher PRA with low sodium dialysate (131 mEq/l). PAC slightly but significantly decreased during dialysis with low sodium dialysate and significantly increased during ultrafiltration. The present results suggest that sodium dialysate concentration has a significant influence on the function of the autonomic system, PRA and PAC in haemodialysed patients.
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PMID:High and low sodium acetate haemodialysis and ultrafiltration. II. Comparison of plasma renin activity (PRA), catecholamine levels (CA) and plasma aldosterone concentration (PAC). 353 26

We compared the effects of 500 ml of 0.15M NaCl or 750 ml of 0.15M NaHCO2, infusions on PRA and PAC in 16 normal NaCl-restricted men. More positive sodium balance, greater natriuresis, and lower serum chloride, potassium, and hydrogen ion concentrations were observed after NaHCO3 infusion. PRA decreased (13.8 +/- 1.0 ng/ml angiotensin I per hour to 6.6 +/- 0.70) and PAC did not change (98 +/- 15 ng/dl to 86 +/- 15) after NaCl infusion. Conversely, PRA did not change (9.9 +/- 1.6 to 10.1 +/- 1.6) and PAC decreased (85 +/- 9 to 44 +/- 5) after NaHCO3 infusion. Plasma cortisol declined in both groups. These results suggest that in sodium-restricted man chloride is more important than sodium for the suppression of PRA by NaCl loading and that potassium or hydrogen ion is a more sensitive modulator of aldosterone secretion than is renin.
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PMID:Renin and aldosterone responses to short-term NaCl or NaHCO3 loading in man. 628 47

Continuous ambulatory peritoneal dialysis (CAPD) entails the continuous presence of hypertonic dialysate in the peritoneal cavity. We postulated that the continuous, gradual ultrafiltration produces chronic activation of the renin-angiotensin system and the adrenal zona glomerulosa. To explore this hypothesis, we measured plasma levels of PRA, active renin (AR), total renin (TR), inactive renin (IR), 18-hydroxycorticosterone (18-OH-B), and aldosterone (PAC) under basal and stimulated conditions. At 0800 and 1200 hr after overnight recumbency, plasma levels of PRA, AR, TR, IR, and 18-OH-B were elevated above the range for sodium-replete recumbent normal subjects. PAC, however, was normal. The increase in TR was due predominantly to an increase in AR. After the combined stimulus of 4 hr ambulation and the ultrafiltration induced by a 2 L exchange, plasma levels of PRA, AR, TR, IR, and PAC were within the range for sodium-replete upright normal subjects. Plasma 18-OH-B levels, however, remained markedly elevated. Graded intravenous infusion of ACTH at rates of 0.03 to 10 ng/min demonstrated that the threshold for an ACTH-stimulated rise in plasma 18-OH-B and PAC is at least as low as that for cortisol and corticosterone. We conclude that CAPD produces activation of the renin-angiotensin system. The high circulating levels of PRA, AR, and, presumably, angiotensin II result in increased secretion of 18-OH-B by the adrenal zona glomerulosa.
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PMID:Plasma 18-hydroxycorticosterone during continuous ambulatory peritoneal dialysis. 631 27

Male Wistar rats received two i.p. injections of morphine-HCl, 2.5 mg/kg at 8.00 a.m. and 2.00 p.m. on the 1st day: the dose was doubled every other day to reach a total daily dose of 40 mg/kg on the 4th day. This schedule was maintained for 12 days. On day 16 the animals received the last injection of morphine, 20 mg/kg. One hour later (9.00 a.m.) six rats were decapitated and PRA, PAC and ACTH were measured by radioimmunoassay. Groups of six rats were killed at 9.00 a.m. on the 1st, 2nd, 5th and the 8th day after morphine withdrawal. Control data for PRA, PAC and ACTH were obtained from eighteen saline-injected rats. Nine out of morphine-treated animals were kept in metabolism cages to investigate simultaneously food and water intake. and renal excretion. Morphine withdrawal after chronic morphine treatment in the rat resulted in antidiuresis and a reduction of electrolyte excretion which were not due to a reduction in water and food intake. The simultaneous increase of PRA and PAC associated with decreased electrolyte excretion indicates that, in addition to antidiuretic hormone, also the renin-aldosterone-system probably play a relevant role in the renal excretory changes after morphine withdrawal.
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PMID:Effect of morphine withdrawal on food and water intake, urine output and electrolyte excretion in the rat: participation of the renin-aldosterone-system in renal excretory changes. 633 Oct 67

To evaluate the role of the central nervous system on the furosemide-induced increases in plasma noradrenaline (PNA), renin activity (PRA), and aldosterone concentration (PAC), central vasoactive sympathetic structures were inhibited by intravertebral artery infusion of colnidine. Intravertebral artery infusion of clonidine (0.06 microgram/Kg/min) significantly reduced basal PNA, heart rate, and arterial pressure, while both PRA and PAC were increased. Intravenous infusion of the same dose of clonidine caused no significant changes in PNA, PRA, and PAC. Intravertebral artery infusion of clonidine (0.02 or 0.1 microgram/Kg/min) significantly suppressed the furosemide-induced increases in PNA and heart rate, and induced a drop in arterial pressure. Although the furosemide-induced increase in PRA was suppressed by intravertebral artery infusion of clonidine, the furosemide-induced increase in PAC was not affected. These results suggest that the furosemide-induced increase in PNA may be mediated by the central sympathetic nervous system and that some of the furosemide-induced increase in PRA may be mediated by central sympathetic neural activation.
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PMID:Contributions of central sympathetic neural activity to furosemide-induced increases in plasma renin activity and noradrenaline. 634 67

Although propranolol administration produces a lowering of PRA, PAC does not decrease in a similar fashion. In the present study the effects of propranolol on the aldosterone MCR were examined. Eight patients with essential hypertension were studied while receiving treatment with a diuretic and again after propranolol (160 to 320 mg/day) was added to the therapeutic regimen. Propranolol therapy was associated with a 25% decrease in PRA (p less than 0.05) and changes in PACs that were variable but not significantly different from diuretic therapy alone. The aldosterone MCR decreased from 1420 +/- 120 to 1120 +/- 90 L/24 hr in response to propranolol (p less than 0.01). The average production rate of aldosterone (MCR X PAC) did not change after propranolol treatment despite a decrease in PRA. There were no changes in plasma concentrations of potassium or in ACTH secretion (as reflected by levels of cortisol) to explain a role for propranolol to sustain aldosterone secretion. Thus propranolol administered to hypertensive patients pretreated with a diuretic can affect circulating levels of aldosterone apart from changes in PRA. Propranolol therapy produces a moderate reduction in aldosterone MCR and appears to augment aldosterone production by a mechanism exclusive of known stimuli.
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PMID:Effects of propranolol on aldosterone plasma concentration and aldosterone metabolic clearance in hypertensive patients. 736 15

The usefulness of the captopril test as a simultaneous screening method for primary aldosteronism (PA) and renovascular hypertension (RVH) was evaluated in 111 patients with essential hypertension, and in 79 patients with secondary hypertension, which included 16 patients with PA and 18 with RVH. Plasma renin activity (PRA, ng/mL/h) and plasma aldosterone concentration (PAC, ng/dL) were determined before and 90 min after administration of 50 mg of captopril in the supine position on a normal NaCl diet. A cutoff point or a discriminant function in the screening was determined by discriminant analysis. A quadratic discriminant function of PRA and PAC after the captopril test identified patients with PA with a false negative rate of 6.3% (1/16), and a false positive rate of 0.6% (1/174) which was significantly lower than that of 3.4% at the basal state (P < .05). In the screening for RVH, the criterion of a postcaptopril PRA of greater than 10.6 ng/mL/h had a false negative rate of 5.6% (1/18) and a false positive rate of 15.1% (26/172). This false positive rate was also significantly lower than that using a criterion for precaptopril PRA of 2.21 ng/mL/h (P < .05). Accordingly, the captopril test was a useful method in the simultaneous screening for PA and RVH, and it may be particularly applicable in specialized hypertension clinics.
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PMID:The usefulness of the captopril test as a simultaneous screening for primary aldosteronism and renovascular hypertension. 830 62


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