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 object of this study was to investigate the renal component of hypertension in aortic constriction. In 40-day-old Sprague-Dawley rats the aorta were constricted either proximal (PAC) or distal (DAC) to the renal arteries. The rats were examined 3 weeks later together with control rats. The arterial pressure proximal to the constriction was elevated in the PAC group but not in the DAC group. In PAC rats the arterial pressure was also elevated distal to the constriction. There was a significant pressure gradient across the constriction in both PAC and DAC rats. The PAC rats had a significant decrease of renal blood flow, a significant increase in renal vascular resistance and a numerical but not significant decrease of glomerular filtration rate. Serum levels of angiotensin II were not significantly different in PAC and control rats. The pressor effect of a bolus dose of angiotensin II was significantly increased in PAC rats. Captopril, a converting enzyme inhibitor, decreased the arterial pressures and renal vascular resistance in PAC rats. The pressure elevating effects of angiotensin II and pressure lowering effect of captopril were more pronounced distal than proximal to the constriction. We conclude that the kidneys play a major role in the development of hypertension in PAC, and that the local effect of angiotensin II on the renal vascular bed is an important contributor to the renal component of the hypertension.
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PMID:Studies of the renal component of the hypertension in rats with aortic constriction. Role of angiotensin II. 352 26

Dose-response curves of blood pressure and of the biochemical components of the renin-angiotensin-aldosterone system were determined during long-term treatment with captopril in 21 hypertensive patients. Captopril was given in biweekly, doubling doses starting with 25 mg 3 times a day until control of blood pressure was achieved or a total daily dosage of 600 mg was reached. Recumbent and standing systolic and diastolic blood pressure fell on 75 mg captopril daily. Increasing the captopril dose did not induce further significant hypotensive effects. The pretreatment level of plasma renin activity (PRA) was a poor predictor of the hypotensive effect of captopril. The rises in PRA and plasma angiotensin I level (PA I) and the decrease in plasma angiotensin II level (PA II) and plasma aldosterone level (PAC) provide biochemical evidence for angiotensin-converting enzyme (ACE) inhibition in vivo. These effects were present on daily doses of 75 to 150 mg captopril.
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PMID:Dose response in captopril therapy of hypertension. 625 Jul 59

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

The studies were designed to explore the effect of the converting enzyme inhibitor captopril on the activity of the sympathetic nervous system during basal conditions and following graded physical exercise in patients with essential hypertension. Seven males and two females, aged 36-59 years, were hospitalized under metabolic ward conditions and treated for 7 days with captopril given orally in increasing dosages, the final dose being 600 mg daily. The patients were subjected to an individual, graded submaximal work test (bicycling) for 20 min before medication and then again in an identical manner during medication with 600 mg captopril. Blood samples were drawn before exercise and then after 10 and 20 min of work for the determination of plasma angiotensin II (PA II), plasma aldosterone (PAC), plasma renin activity (PRA), plasma noradrenaline (PNA) and plasma adrenaline (PA). Before medication blood pressure (mmHg) was 195/133 immediately before exercise, 230/129 after 10 min of moderate exercise and 263/105 following 20 mon of nearly maximal work. During treatment with captopril the respective blood pressure values were 154/110, 200/100 and 245/98. Captopril had no significant effect on the changes in heart rate following physical exercise. PA II and PAC were substantially reduced and PRA considerably increased by captopril. PA II, PAC and PRA increased in response to exercise both before and following captopril. The exercise stimulated increase in PNA and PA was almost identical before and during captopril. Thus, captopril had no major effect on the activity of the sympathetic nervous system in patients with essential hypertension, neither during basic conditions nor during heavy physical exercise in spite of a profound decrease in PA II.
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PMID:The effect of captopril on catecholamines, renin activity, angiotensin II and aldosterone in plasma during physical exercise in hypertensive patients. 680 Aug 10