Vierhapper H, Waldhäusl W
Eur J Clin Invest. 1982 Jun;12(3):263-7. doi: 10.1111/j.1365-2362.1982.tb01002.x.
The pressor response to both angiotensin II (5, 10 and 20 ng kg-1 min-1) and to noradrenaline (50, 100 and 200 ng kg-1 min-1) was reduced (P less than 0.05 to less than 0.005) in six healthy male subjects following the administration of the calcium-antagonist nifedipine (10 mg p.o.). Nifedipine induced a rise in basal plasma noradrenaline concentrations but did not alter the plasma concentrations of adrenaline, dopamine, renin and aldosterone. A slight reduction in the angiotensin II induced rise of plasma aldosterone by nifedipine was observed after the administration of the largest dose of angiotensin II only (P less than 0.05). The reduced responsiveness towards pressor agents following oral nifedipine is in keeping with the known antihypertensive effect of calcium-antagonistic drugs and could provide a concept for the effectiveness of these drugs in hypertensive crisis.
在六名健康男性受试者口服钙拮抗剂硝苯地平(10毫克)后,对血管紧张素II(5、10和20纳克/千克/分钟)和去甲肾上腺素(50、100和200纳克/千克/分钟)的升压反应均降低(P小于0.05至小于0.005)。硝苯地平使基础血浆去甲肾上腺素浓度升高,但未改变肾上腺素、多巴胺、肾素和醛固酮的血浆浓度。仅在给予最大剂量血管紧张素II后,观察到硝苯地平使血管紧张素II诱导的血浆醛固酮升高略有降低(P小于0.05)。口服硝苯地平后对升压药反应性降低与钙拮抗药物已知的降压作用相符,并可为这些药物在高血压危象中的有效性提供一种解释。