Hyman A L, Lippton H L, Kadowitz P J
Fed Proc. 1986 Aug;45(9):2336-40.
The subtypes of postjunctional alpha adrenoceptors in the feline pulmonary vascular bed were studied by using selective alpha-adrenoceptor agonists and antagonists. Under conditions of controlled pulmonary blood flow and constant left atrial pressure, intralobar injections of the alpha 1 agonists phenylephrine and methoxamine, and the alpha 2 agonists UK 14,304 and B-HT 933, increased lobar arterial pressure in a dose-related manner. Prazosin, an alpha 1-adrenoceptor antagonist, reduced responses to phenylephrine and methoxamine to a greater extent than responses to UK 14,304 and B-HT 933. Yohimbine, an alpha 2 blocker, decreased responses to UK 14,304 and B-HT 933 without altering responses to phenylephrine or methoxamine. The same pattern of blockade was observed in animals pretreated with 6-hydroxydopamine, an adrenergic neuronal blocking agent. However, in propranolol-treated animals, prazosin antagonized responses to phenylephrine and methoxamine without altering responses to UK 14,304 or B-HT 933, and the selectivity of the blocking effects of yohimbine were preserved. Responses to intralobar injections of norepinephrine (NE) were markedly decreased by prazosin, whereas yohimbine had only a small effect. These data suggest the presence of both postjunctional alpha 1 and alpha 2 adrenoceptors mediating vasoconstriction in the pulmonary vascular bed. These results also indicate that the vasoconstrictor responses to injected NE in the cat pulmonary vascular bed result mainly from activation of alpha 1 adrenoceptors.
利用选择性α-肾上腺素能受体激动剂和拮抗剂,对猫肺血管床中节后α-肾上腺素能受体的亚型进行了研究。在肺血流量受控和左心房压力恒定的条件下,叶内注射α1激动剂去氧肾上腺素和甲氧明,以及α2激动剂UK 14,304和B-HT 933,可使叶动脉压呈剂量依赖性升高。α1-肾上腺素能受体拮抗剂哌唑嗪对去氧肾上腺素和甲氧明反应的抑制程度大于对UK 14,304和B-HT 933反应的抑制程度。α2阻滞剂育亨宾可降低对UK 14,304和B-HT 933的反应,而不改变对去氧肾上腺素或甲氧明的反应。在用肾上腺素能神经元阻滞剂6-羟基多巴胺预处理的动物中也观察到了相同的阻断模式。然而,在普萘洛尔处理的动物中,哌唑嗪拮抗了对去氧肾上腺素和甲氧明的反应,而不改变对UK 14,304或B-HT 933的反应,并且育亨宾的阻断作用选择性得以保留。哌唑嗪可显著降低叶内注射去甲肾上腺素(NE)的反应,而育亨宾的作用较小。这些数据表明肺血管床中存在介导血管收缩的节后α1和α2肾上腺素能受体。这些结果还表明,猫肺血管床中对注射NE的血管收缩反应主要源于α1肾上腺素能受体的激活。