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用卡替洛尔进行β受体阻滞对去甲肾上腺素能而非血管紧张素能血压控制的调节作用。

Modulation of noradrenergic but not angiotensinergic blood pressure control by beta-blockade with carteolol.

作者信息

Saxenhofer H, Morger D, Weidmann P, Ferrier C, Shaw S G

机构信息

Medizinische Poliklinik, University of Bern, Switzerland.

出版信息

J Hypertens. 1991 Nov;9(11):1049-56. doi: 10.1097/00004872-199111000-00011.

Abstract

Various beta-blockers possessing similar antihypertensive potency have been found to differ widely with regard to their influence on blood pressure-regulating factors such as cardiac output and plasma levels of renin or norepinephrine. Recently, beta-blocker-induced stimulation of circulating atrial natriuretic factor (ANF) was reported. Blood pressure is determined not only by levels of vasoconstrictive factors but also by tissue reactivity. To investigate these aspects, we assessed the cardiovascular responsiveness to norepinephrine and angiotensin II, plasma levels of catecholamines, angiotensin II, ANF and aldosterone and the body sodium-blood volume state of 15 patients with essential hypertension (mean age +/- s.e.m., 42 +/- 3 years) and 12 normal control subjects (41 +/- 5 years), first on placebo and then after 4 weeks of intervention with carteolol, a non-selective beta-adrenergic antagonist with intrinsic sympathomimetic activity. Compared with placebo, carteolol decreased resting plasma norepinephrine in both groups while plasma norepinephrine-blood pressure response curves were shifted to the left, their slopes increased and norepinephrine pressor doses decreased (P less than 0.05 to less than 0.001). Chronotropic responses to isoproterenol were abolished but negative chronotropic responses to a norepinephrine-induced 20 mmHg rise in diastolic blood pressure were unaltered. Plasma norepinephrine clearance in the supine position was slightly decreased in hypertensive and unchanged in normal subjects. Supine and upright blood pressure was lowered (P less than 0.05 to 0.001) in the hypertensive while upright systolic blood pressure only decreased in the normal group.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

已发现各种具有相似降压效力的β受体阻滞剂在对诸如心输出量、肾素或去甲肾上腺素血浆水平等血压调节因子的影响方面存在很大差异。最近,有报道称β受体阻滞剂可刺激循环中的心房利钠因子(ANF)。血压不仅取决于血管收缩因子的水平,还取决于组织反应性。为了研究这些方面,我们评估了15例原发性高血压患者(平均年龄±标准误,42±3岁)和12例正常对照者(41±5岁)对去甲肾上腺素和血管紧张素II的心血管反应性、儿茶酚胺、血管紧张素II、ANF和醛固酮的血浆水平以及身体钠血容量状态,首先在服用安慰剂时进行评估,然后在使用具有内在拟交感活性的非选择性β肾上腺素能拮抗剂卡替洛尔干预4周后进行评估。与安慰剂相比,卡替洛尔使两组患者静息血浆去甲肾上腺素水平降低,而去甲肾上腺素-血压反应曲线向左移动,其斜率增加,去甲肾上腺素升压剂量降低(P小于0.05至小于0.001)。对异丙肾上腺素的变时反应被消除,但对去甲肾上腺素引起的舒张压升高20 mmHg的负性变时反应未改变。高血压患者仰卧位血浆去甲肾上腺素清除率略有降低,正常受试者则无变化。高血压患者仰卧位和直立位血压均降低(P小于0.05至0.001),而正常组仅直立位收缩压降低。(摘要截短于250字)

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