Polonia J J, Monteiro A, Esteves A, Cunha M E, Santos M L, Coutinho J, Coelho J L, Brandao F A, Cerqueira-Gomes M
Unidade de Farmacologia Clinica, Hospital de S. Joao, Faculdade de Medicina, Porto, Portugal.
Am J Med. 1988 Mar 11;84(3A):148-51. doi: 10.1016/0002-9343(88)90223-9.
Experimental evidence of captopril-induced inhibition of sympathetic activity, mediated by decrease in angiotensin II production, is presented. The blood pressure, plasma catecholamine, plasma renin activity, and plasma aldosterone responses to a single dose of sublingual captopril in 23 patients with hypertensive emergencies were evaluated. The major correlation found was between the captopril-induced decrease in blood pressure and the decrease in plasma norepinephrine levels (r = 0.57, p less than 0.01). In another 11 hypertensive patients with normal or high renin levels, captopril lowered by 65 percent the increase in plasma norepinephrine induced by cold immersion of the forearm. In both circumstances, plasma renin and aldosterone levels changed in accordance with the expected inhibition of angiotensin converting enzyme activity. These data suggest that, in selected circumstances in hypertensive patients, captopril exhibits a depressive influence on sympathetic activity along with the inhibition of the renin-angiotensin system.
本文提供了卡托普利通过降低血管紧张素II生成介导的抑制交感神经活动的实验证据。评估了23例高血压急症患者单次舌下含服卡托普利后的血压、血浆儿茶酚胺、血浆肾素活性和血浆醛固酮反应。发现的主要相关性在于卡托普利引起的血压下降与血浆去甲肾上腺素水平下降之间(r = 0.57,p < 0.01)。在另外11例肾素水平正常或升高的高血压患者中,卡托普利使前臂冷浸诱导的血浆去甲肾上腺素增加降低了65%。在这两种情况下,血浆肾素和醛固酮水平均按照血管紧张素转换酶活性的预期抑制而变化。这些数据表明,在高血压患者的特定情况下,卡托普利除了抑制肾素-血管紧张素系统外,还对交感神经活动具有抑制作用。