Why the study?
Does captopril administration alter mean blood pressure and neurohormonal markers in patients with essential hypertension?
Does captopril administration alter mean blood pressure and neurohormonal markers in patients with essential hypertension?
The blood pressure lowering effect of captopril does not perfectly correlate with its blood levels, suggesting complex short- and long-acting mechanisms.
The time courses of mean blood pressure (MBP), plasma renin activity (PRA), plasma aldosterone (PA), serum prostaglandin E (PGE), serum angiotensin I converting enzyme (ACE), and blood levels of angiotensin I converting enzyme inhibitor (SQ 14,225) (captopril) were studied in 6 patients with essential hypertension (5 men and 1 woman, aged 44 +/- 5.6 (mean +/- S.E.) years) before and 30, 60, 120 and 180 min after administration of 25 mg captopril. MBP and ACE began to fall within 30 min and reached a significant minimum between 60 and 180 min after captopril administration. PRA was significantly increased 60 min after captopril administration and continued for 180 min. On the other hand, PA had begun to fall significantly 180 min after captopril administration. The blood levels of captopril were significantly increased 30 min after captopril administration, with a peak at 120 min. The levels at 180 min were half the peak. The levels of PGE were not significantly changed within 180 min after captopril administration. These results suggest a discrepancy between the changes in MBP and the blood levels of captopril. The blood pressure lowering effect may be due to inhibition of angiotensin II (Ang. II) during the short-acting effect, and due to decrease of PA, metabolites of captopril, increase of kinin in the blood, inhibition of the slow pressor effect of Ang. II, increases of other depressor hormones such as prostacyclin and other depressor mechanisms during the long-acting effect.
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Honda et al. (1981) studied this question.
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