Key result
ACE inhibitors lower blood pressure and raise plasma kinins in essential hypertension.
Why the study?
The role of the kallikrein-kinin system in the hypotensive mechanisms of angiotensin I converting enzyme inhibitors in essential hypertension was unclear.
Do angiotensin I converting enzyme inhibitors affect the kallikrein-kinin system to lower blood pressure in patients with essential hypertension?
Do angiotensin I converting enzyme inhibitors affect the kallikrein-kinin system to lower blood pressure in patients with essential hypertension?
The hypotensive effect of ACE inhibitors in essential hypertension may be mediated by increased plasma kinins, particularly in low-renin patients where angiotensin II levels do not significantly change.
May implicate kinins in ACE inhibitor BP reduction in low-renin hypertension; hypothesis-generating and requires prospective validation before practice change.
Patients with essential hypertension were studied to clarify the role of the kallikrein-kinin system in the hypotensive actions of angiotensin I converting enzyme inhibitors. Captopril, alacepril, ramipril, and altiopril administered in single doses rapidly decreased blood pressure and plasma angiotensin II levels, and increased plasma and urinary kinins as well as plasma renin activity. Following administration of captopril for 14 days, similar effects were observed. Urine volume and urinary sodium excretion were augmented after acute and chronic administration of captopril. The patients who received ramipril and altiopril were divided into renin subgroups. In the normal-renin group, the change in blood pressure was accompanied by an increase in plasma kinin level and a decrease in plasma angiotensin II level. However, in the low-renin group, although these drugs reduced blood pressure and increased plasma kinin, no significant change was observed in plasma angiotensin II levels. These findings suggest that (a) in patients with normal renin activity, the hypotensive effect of converting enzyme inhibitors might be caused by an increase in plasma kinin and a decrease in plasma angiotensin II, but in the low-renin group, the increase in plasma kinin levels may be more important; and (b) the augmentation of urine volume and urinary sodium excretion may also be related to the hypotensive effects of the converting enzyme inhibitors during long-term administration.
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Iimura et al. (1989) studied Essential hypertension. Angiotensin I converting enzyme inhibitors (Captopril, alacepril, ramipril, altiopril) was evaluated on Blood pressure, plasma angiotensin II levels, plasma and urinary kinins, and plasma renin activity. Angiotensin I converting enzyme inhibitors decreased blood pressure and increased plasma kinins in patients with essential hypertension, with differing effects on angiotensin II based on renin status.
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