Elliott H L, Donnelly R, Reid J L
University Department of Materia Medica, Stobhill General Hospital, Glasgow, U.K.
J Cardiovasc Pharmacol. 1988;11 Suppl 1:S62-6.
The principal aim of this study was to investigate the effects of ketanserin on peripheral vascular pressor mechanisms in nine patients with essential hypertension, including an assessment of the responsiveness to intravenous infusions of the alpha 1-adrenergic agonist, phenylephrine, and the nonadrenergic vasoconstrictor, angiotensin II. There were small but significant rightward shifts in the phenylephrine pressor dose-response curves (by 1.5- to twofold) following ketanserin but no shifts for angiotensin II. This modest shift in phenylephrine responsiveness contrasted with the fivefold shift obtained with a single oral dose (1 mg) of prazosin. The relationship between the phenylephrine-induced increase in blood pressure and the reduction in heart rate was used as an index of baroreflex responsiveness: there were no significant effects attributable to ketanserin. There were no significant differences in plasma aldosterone or renin activity, nor in 24-h urinary volume or electrolytes, following ketanserin. The principal mechanism underlying the antihypertensive effect of ketanserin is unlikely to involve peripheral vascular alpha 1-adrenoceptor antagonism, altered baroreflex responsiveness, or perturbation of the renin-angiotensin-aldosterone system.
本研究的主要目的是调查酮色林对9例原发性高血压患者外周血管升压机制的影响，包括评估对静脉输注α1 - 肾上腺素能激动剂去氧肾上腺素和非肾上腺素能血管收缩剂血管紧张素II的反应性。酮色林给药后，去氧肾上腺素升压剂量 - 反应曲线有小但显著的右移（1.5至两倍），而血管紧张素II的曲线无移位。去氧肾上腺素反应性的这种适度变化与单次口服剂量（1毫克）哌唑嗪引起的五倍变化形成对比。去氧肾上腺素引起的血压升高与心率降低之间的关系被用作压力反射反应性的指标：酮色林对此无显著影响。酮色林给药后，血浆醛固酮或肾素活性、24小时尿量或电解质均无显著差异。酮色林降压作用的主要机制不太可能涉及外周血管α1 - 肾上腺素能受体拮抗、压力反射反应性改变或肾素 - 血管紧张素 - 醛固酮系统的扰动。
