Enhancement of alpha- and beta-adrenoceptor responses by elevations in vascular tone in pulmonary circulation.
Enhancement of alpha- and beta-adrenoceptor responses by elevations in vascular tone in pulmonary circulation.
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通过肺循环中血管张力的升高来增强α-和β-肾上腺素受体反应。
DOI：
10.1152/ajpheart.1986.250.6.h1109
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发表时间：
1986
期刊：
影响因子：
--
通讯作者：
Kadowitz,PJ
中科院分区：
文献类型：
--
作者：
Hyman,AL;Kadowitz,PJ
在猫肺血管床中研究了血管张力增加对选择性α 1-和α 2-肾上腺素受体激动剂、去甲肾上腺素、肾上腺素和异丙肾上腺素反应的影响。在静息张力条件下，肺血流和左心房压力恒定，叶内注射α 1-肾上腺素能受体激动剂，苯肾上腺素和甲氧胺，和α 2-肾上腺素能受体激动剂，UK 14304和B-HT 933，增加叶动脉压。当肺血管阻力升高到一个高的稳定水平时，对α 2-肾上腺素受体激动剂的血管收缩反应明显增加，对甲氧胺的反应在较小程度上增加，对苯肾上腺素和肾上腺素的升压反应被逆转。这些血管舒张反应苯肾上腺素和肾上腺素在血管张力升高被阻断普萘洛尔。此外，在β-肾上腺素受体阻滞后，对苯肾上腺素、肾上腺素和去甲肾上腺素的血管收缩反应在升高的张力下也比在静息张力下大。血管舒张反应的β-肾上腺素能受体兴奋剂，异丙肾上腺素，增强在更高水平的血管收缩张力，并阻止普萘洛尔和沙丁胺醇，选择性β 2-肾上腺素能受体拮抗剂。对α 2-肾上腺素能受体激动剂的血管收缩反应的增强被育亨宾选择性地阻断，而对α 1-肾上腺素能受体激动剂的血管收缩反应的增强以及对去甲肾上腺素和肾上腺素的血管收缩反应的大部分被哌唑嗪阻断。目前的数据支持的假设，postjunctional α 1-和α 2-肾上腺素受体介导的血管收缩和β 2-肾上腺素受体介导的血管舒张存在于猫肺血管床。（250字处删节）
The influence of increases in vascular tone on responses to selective alpha 1- and alpha 2-adrenoceptor agonists, norepinephrine, epinephrine, and isoproterenol was investigated in the feline pulmonary vascular bed. Under resting tone conditions with constant pulmonary blood flow and left atrial pressure, intralobar injections of the alpha 1-adrenoceptor agonists, phenylephrine and methoxamine, and the alpha 2-adrenoceptor agonists, UK 14304 and B-HT 933, increased lobar arterial pressure. When pulmonary vascular resistance was raised to a high steady level, vasoconstrictor responses to the alpha 2-adrenoceptor agonists were markedly increased, responses to methoxamine were increased to a lesser extent, and pressor responses to phenylephrine and epinephrine were reversed. These vasodilator responses to phenylephrine and epinephrine at elevated vascular tone were blocked by propranolol. Moreover, after beta-adrenoceptor blockade, vasoconstrictor responses to phenylephrine, epinephrine, and norepinephrine were also greater at elevated tone than at resting tone. Vasodilator responses to the beta-adrenoceptor stimulant, isoproterenol, were enhanced at higher levels of vasoconstrictor tone and were blocked by propranolol and by albuterol, a selective beta 2-adrenoceptor antagonist. The enhanced vasoconstrictor responses to the alpha 2-adrenoceptor agonists were selectively blocked by yohimbine, whereas the enhanced responses to the alpha 1-adrenoceptor agonists and, for the most part, the vasoconstrictor responses to norepinephrine and epinephrine, were blocked by prazosin. The present data support the hypothesis that postjunctional alpha 1- and alpha 2-adrenoceptors mediating vasoconstriction and beta 2-adrenoceptors mediating vasodilation are present in the feline pulmonary vascular bed.(ABSTRACT TRUNCATED AT 250 WORDS)