Mills P, Dimsdale J, Ziegler M, Brown M
Department of Psychiatry, University of California, San Diego, La Jolla 92093.
Clin Exp Hypertens A. 1990;12(2):179-90. doi: 10.3109/10641969009074727.
Adding converting-enzyme inhibitors to the salt depleted state is marked by a reduction in blood pressure despite compensatory increases in heart rate and plasma norepinephrine. This study investigated whether this increase in sympathetic function is also accompanied by an increase in beta-adrenergic receptor function. Ten subjects were studied following two separate five day hospitalizations on 10 mEq sodium diets while receiving either placebo or captopril. During low sodium with captopril, blood pressure and angiotensin II decreased, while heart rate, renin, norepinephrine and isoproterenol-stimulated cyclic AMP accumulation in lymphocytes increased. The results indicate that enhanced beta-adrenergic receptor function does accompany sympathetic activation during sodium restriction and converting enzyme inhibition and further support studies showing that the renin-angiotensin system plays the dominant role in blood pressure regulation in the sodium depleted state.
在盐缺失状态下添加转换酶抑制剂，尽管心率和血浆去甲肾上腺素出现代偿性升高，但血压仍会降低。本研究调查了交感神经功能的这种增强是否也伴随着β-肾上腺素能受体功能的增加。在10名受试者分别接受为期5天的住院治疗期间，给予10 mEq的钠饮食，同时服用安慰剂或卡托普利。在低钠饮食且服用卡托普利期间，血压和血管紧张素II降低，而心率、肾素、去甲肾上腺素以及异丙肾上腺素刺激的淋巴细胞中环磷酸腺苷（cAMP）积累增加。结果表明，在钠限制和转换酶抑制过程中，交感神经激活确实伴随着β-肾上腺素能受体功能增强，进一步支持了表明肾素-血管紧张素系统在盐缺失状态下的血压调节中起主导作用的研究。
