Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033036 (APC)
 10,214 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The new angiotensin converting enzyme inhibitor enalapril maleate was given in single oral doses of 2.5, 5, and 10 mg to 11 hospitalized patients with uncomplicated essential hypertension who were on a 150-mEq sodium diet. All doses of enalapril induced reduction of mean seated diastolic blood pressure (SDBP). The magnitude of the initial SDBP reduction was not dose related, but the duration of effect was longer (greater than 12 hr) after the 5 and 10 mg. After dosing, mean plasma angiotensin converting enzyme activity (ACE) and aldosterone concentration (PAC) fell, while plasma renin activity (PRA) rose. Serum concentrations of the active diacid from of enalapril increased linearly with dosage; ACE was inhibited maximally at concentrations above 10 ng/ml. During repeated dosing in the outpatient trial there was attenuation of the antihypertensive effect (12 to 24 hr after dosing) in eight of 10 patients. Despite dose increases only two patients achieved SDBP control (less than or equal to 90 mm Hg). In the five patients in whom 50 mg/day hydrochlorothiazide was added near the end of the trail mean SDBP was further reduced. Enalapril was well tolerated. Further studies of the drug, especially in combination with diuretic, are needed.
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PMID:Effects of enalapril, a new converting enzyme inhibitor, in hypertension. 628 27

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

The renin-angiotensin system was studied in eight patients with Cushing's syndrome (four with adrenal adenoma and four with adrenal hyperplasia) and in five normal controls. Basal plasma renin activity (PRA) and aldosterone concentration (PAC) were similar in supine position among Cushing's syndrome due to adrenal adenoma (PRA; 1.0 +/- 0.3 ng/ml/h, PAC; 7.4 +/- 1.0 ng/dl, mean +/- SE), those due to adrenal hyperplasia (1.0 +/- 0.2, 6.9 +/- 0.8) and the controls (0.8 +/- 0.1, 6.4 +/- 0.4). The PRA after furosemide (1 mg/kg i.v.) and 120 min. upright posture stimulation was similar among Cushing's syndrome due to adrenal adenoma (2.2 +/- 0.7 ng/ml/h), those due to adrenal hyperplasia (2.6 +/- 1.7) and the controls (2.5 +/- 1.2). However, the PAC response after the stimulation in Cushing's syndrome due to adrenal hyperplasia (7.1 +/- 1.2 ng/dl) was significantly lower than that in the controls (17.5 +/- 2.1) (p less than 0.01), although there was no significant difference between the PAC response in Cushing's syndrome due to adrenal adenoma (12.6 +/- 1.0) and the controls. These results indicate that PAC response to furosemide and upright pasture stimulation might be suppressed in Cushing's syndrome due to adrenal hyperplasia.
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PMID:Renin-angiotensin system and plasma aldosterone in Cushing's syndrome. 632 49

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

This study explores the hypothesis that the continuous ultrafiltration that accompanies continuous ambulatory peritoneal dialysis (CAPD) produces greater activation of the renin-angiotensin aldosterone axis than does the intermittent ultrafiltration that accompanies thrice weekly hemodialysis (HD). Plasma renin activity (PRA), active renin (AR), total renin (TR), inactive renin (IR), 18-hydroxycorticosterone (18-OH-B), aldosterone (PAC), and cortisol were measured in plasma from CAPD (n = 6) and HD (n = 10) patients. Blood from CAPD patients was sampled at 8 AM after overnight recumbency and at 12 noon after four hours ambulation. Blood from HD patients was sampled immediately pre-HD (8 AM) and post-HD (12 noon) at both 8 AM and 12 noon. PRA (P less than 0.01), AR (P less than 0.01), and AR/TR (100%; P less than 0.01) were higher in CAPD than in HD. IR and TR were not different in the two groups. Plasma 18-OH-B was normal in HD but markedly elevated in CAPD. 18-OH-B was higher in CAPD than in HD at 8 AM (P less than 0.05) and at 12 noon (P less than 0.05). Plasma cortisol was not different in the two groups. We conclude that the greater degree of renin activation in CAPD versus HD contributes to the higher levels of 18-OH-B and PAC observed in CAPD patients.
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PMID:Plasma concentrations of 18-hydroxycorticosterone and aldosterone in continuous ambulatory peritoneal dialysis and hemodialysis patients. 635 94

Urinary excretion of prostaglandin E2 (PGE2) and F2 alpha (PGF2 alpha), plasma concentrations of renin (PRC), aldosterone (PAC), noradrenaline (PNA) and adrenaline (PA) were determined in the third trimester of pregnancy, 5 days and 3 months after delivery in preeclampsia and normotensive pregnant and non-pregnant control subjects. PGE2 was higher in pregnant control subjects than in non-pregnant subjects, but reduced to non-pregnant level in preeclampsia. PGF2 alpha was the same in preeclampsia and normotensive pregnancy but higher than in the non-pregnant group. PRC and PAC were increased during pregnancy, but considerably lesser in preeclampsia than during normotensive pregnancy. PNA and PA were the same in all three groups. All parameters were normal 3 months after delivery. There were no correlations between any of the hormones and blood pressure in any of the groups. PGE2 was positively correlated to PRC. The lack of renal PGE2 in preeclampsia might be responsible for the decrease in renal blood flow and sodium excretion, and the changes in PRC and PAC are supposed to be secondary to changes in PGE2. It is hypothesised that preeclampsia is a state of prostaglandin deficiency.
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PMID:Prostaglandins, renin, aldosterone, and catecholamines in preeclampsia. 636 75

In order to evaluate the effect of the angiotensin I-converting enzyme inhibitor, captopril, on lipid metabolism, we measured serum lipoperoxides concentration ( LPX ) as well as plasma levels of renin activity (PRA), aldosterone (PAC) and bradykinin ( PBK ) before and after captopril administration in 15 hypertensive patients. Captopril significantly lowered the LPX (p less than 0.05 by repeated measures ANOVA) from the control value of 3.25 +/- 1.16 (mean +/- S.D.) to 2.92 +/- 0.94, 2.83 +/- 1.10, and 2.89 +/- 1.31 nmol/ml 30, 60, and 120 min after the administration, respectively. A significant reduction of blood pressure (p less than 0.0001) and PAC (p less than 0.01) was observed following captopril administration, while PBK increased significantly (p less than 0.001) from a baseline level of 10.85 +/- 4.07 to 13.95 +/- 5.29, 16.25 +/- 6.85, and 15.71 +/- 7.65 pg/ml 30, 60, and 120 min after captopril administration, respectively. There was no significant correlation between changes in serum LPX and in mean blood pressure, PRA and PAC, though a significant inverse relationship was found between changes in serum LPX and in PBK 120 min after the administration (r = -0.576, p less than 0.05, n = 13). Although the mechanisms by which serum LPX is decreased by captopril are not clear, it is suggested from the results that captopril is a beneficial antihypertensive agent for preventing LPX -induced atherosclerosis in hypertensive patients.
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PMID:[The effects of the angiotensin I-converting enzyme inhibitor, captopril, on serum lipoperoxides level and the renin-angiotensin-aldosterone and kallikrein-kinin systems in hypertensive patients]. 637 99

Two patients with systemic lupus erythematosus (SLE) and hyperkalemia were studied. The hyperkalemia was disproportionate to the degree of renal excretory impairment. The usual causes of hyperkalemia were excluded. Basal levels of plasma renin activity (PRA) and plasma aldosterone (PAC) were low. The responses of PRA and plasma aldosterone to the combined stimulus of ambulation and furosemide were blunted. Plasma levels of 18-hydroxycorticosterone (18-OH-B) were normal. The hyperkalemia in both patients could be attributed to hyporeninemic hypoaldosteronism (HH). In one patient, the hyperkalemia was corrected by the administration of fludrocortisone. In the second patient, treatment of lupus nephritis with azathioprine, prednisone, and plasmapheresis normalized both the serum creatinine and the serum potassium.
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PMID:Hyporeninemic hypoaldosteronism in two patients with systemic lupus erythematosus. 637 83


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