Why the study?
Does SQ 20.881 intravenously reduce blood pressure and alter kinin, renin-angiotensin-aldosterone, and catecholamine levels in sodium replete hypertensive patients?
Does SQ 20.881 intravenously reduce blood pressure and alter kinin, renin-angiotensin-aldosterone, and catecholamine levels in sodium replete hypertensive patients?
Inhibition of converting enzyme by SQ 20.881 reduces blood pressure in hypertensive patients primarily through decreased formation of angiotensin II rather than reduced degradation of kinins.
Answers are grounded in this paper and cite their sources.
May support angiotensin II suppression over kinin effects as the dominant ACE-inhibitor mechanism; leaves open confirmation in randomized trials.
Nine sodium replete hypertensive patients with normal or high plasma renin activity (PRA) were given SQ 20.881, 1 mg/kg intravenously BP fell significantly within 20 min and reached its lowest level after 60 min. Blood kinins showed a minor but significant decrease after 60 and 105 min. Plasma angiotensin II was markedly reduced after 15 and 60 min. PRA was significantly increased after 15-105 min. Plasma aldosterone was reduced at 60 min in eight patients and slightly increased in one. Plasma noradrenaline increased after 15 min, whereas adrenaline decreased after 60 min. These results indicate that the reduction of BP following inhibition of converting enzyme by SQ 20.881, 1 mg/kg, is not related to reduced degradation of kinins but rather to decreased formation of angiotensin II. Angiotensin II appears to be of importance for the maintenance of BP in sodium replete hypertensive patients with normal or high PRA.
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Hulthén et al. (1978) studied this question.
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