The effect of captopril mediated afterload reduction on aortic regurgitation was investigated in 10 patients. Regurgitation was quantitated by means of the regurgitation fraction and the relation of regurgitant volume to end diastolic volume. These variables were derived from gated radionuclide ventriculography. After captopril treatment the blood concentration of angiotensin I rose whereas that of angiotensin II fell significantly. The conversion of angiotensin I to II was reduced to about 50% of the control value. Whereas blood pressure and heart rate did not change significantly, the regurgitation fraction and the regurgitant volume, normalised to end diastolic volume, were significantly reduced by captopril treatment. The ejection fraction remained essentially unchanged. These findings suggest that captopril reduces aortic regurgitation by reducing afterload.

In low- and normal- renin hypertensive patients, but not in high-renin patients, the acute antihypertensive response to the angiotensin-converting enzyme (ACE) inhibitor captopril was completely blocked by aprotinin-induced kallikrein inhibition. Blood pressure reduction with long-term ACE inhibition could be overcome only in part by aprotinin. It is proposed that in low- and normal-renin hypertension the vasodepressor effect of acute ACE inhibition is mainly due to kinin accumulation. Conversely, in high-renin patients a fall in angiotensin II concentration accounts for the hypotensive response to captopril. From the pressor effect of aprotinin in chronically captopril treated patients it appears that kinins are also involved in the blood pressure reduction with long-term ACE inhibition. The finding that ACE inhibition and kallikrein blockade produced predictable and opposite effects on blood pressure suggests broad participation of changes in depressor kinin production in the control of vascular tone in essential hypertension.

1. The effect of.aprotinin-induced blockade of the kallikrein-kinin system on haemodynamic and biochemical responses to converting enzyme inhibition by SQ 14 225 was evaluated in 26 patients with essential hypertension.2. SQ 14 225 lowered blood pressure in high, normal and low renin hypertension. In low and normal renin patients, but not in high renin patients, the acute blood pressure-lowering effect of SQ 14 225 could be overcome by aprotinin. Aprotinin infusion produced small vasopressor effects in all groups of patients. 3. Aprotinin lowered the level of circulating active renin but not that of inactive renin. 4. It is concluded that in low and normal, but not in high, renin hypertensive patients activation of the kallikrein-kinin system is responsible for the acute blood pressure reduction observed with converting enzyme inhibition.5. With long-term converting enzyme inhibition kallikrein-kinin system activation seems to play only a minor role.6. The kallikrein-kinin system may be involved in the regulation of blood pressure.7. There is no direct evidence of a participation of kallikrein in the activation of prorenin in vivo.

1. Six weeks' treatment with labetalol (600 mg/day) significantly reduced systolic and diastolic blood pressures in 24 patients with essential hypertension. There was a small but not significant decrease in heart rate. 2. After 6 weeks of therapy mean digital arterial blood flow at rest and during reactive hyperaemia had increased by 26%. 3. In nine essential hypertensive patients intravenous administration of 100 mg of labetalol caused prompt and striking reductions of systolic and diastolic blood pressures without significant changes in heart rate. There was a consistent and significant increase in peripheral blood flow by 32% 5 min after administration of the drug. 4. Antagonism of alpha-receptors in addition to beta-receptors might improve peripheral arterial blood flow while achieving antihypertensive control. Thus labetalol, owing to its favourable haemodynamic effects, may have advantages over conventional pure beta-receptor-blocking agents.

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