Jie K, van Brummelen P, Vermey P, Timmermans P B, van Zwieten P A
Department of Nephrology, University Hospital, Leiden, The Netherlands.
J Hypertens Suppl. 1985 Dec;3(3):S89-91.
Alpha 1- and alpha 2-adrenoceptor mediated vasoconstriction were compared between 13 patients with essential hypertension and 13 normotensive controls, matched for age and sex. For this purpose changes in forearm blood flow induced by infusion of the selective alpha 1-adrenoceptor agonist methoxamine, the selective alpha 2-adrenoceptor agonist B-HT 933, the catecholamines adrenaline and noradrenaline and the alpha 2-adrenoceptor antagonist yohimbine were measured in both study groups. The catecholamines were infused together with propranolol to avoid beta-adrenergic effects. Forearm blood flow was measured by plethysmography. All agonists produced a dose-dependent vasoconstriction which was more pronounced in the hypertensive subjects but no preference was found for either the alpha 1- or alpha 2-adrenoceptor mediated vasoconstriction. Yohimbine induced a greater vasodilatation in the normotensive subjects. The greater vasoconstriction in the hypertensive patients could be explained by structural vascular changes. No evidence was found for an important role of alpha 2-adrenoceptor mediated vasoconstriction in essential hypertension.
在13例原发性高血压患者和13例年龄与性别相匹配的血压正常对照者之间，比较了α1和α2肾上腺素能受体介导的血管收缩作用。为此，在两个研究组中均测量了输注选择性α1肾上腺素能受体激动剂甲氧明、选择性α2肾上腺素能受体激动剂B-HT 933、儿茶酚胺肾上腺素和去甲肾上腺素以及α2肾上腺素能受体拮抗剂育亨宾后引起的前臂血流量变化。儿茶酚胺与普萘洛尔一起输注以避免β肾上腺素能效应。通过体积描记法测量前臂血流量。所有激动剂均产生剂量依赖性血管收缩，在高血压受试者中更为明显，但未发现对α1或α2肾上腺素能受体介导的血管收缩有偏好。育亨宾在血压正常受试者中引起更大的血管舒张。高血压患者中更大的血管收缩可能由血管结构变化来解释。未发现α2肾上腺素能受体介导的血管收缩在原发性高血压中起重要作用的证据。
