Coronary vasoconstriction mediated by alpha 1- and alpha 2-adrenoceptors in conscious dogs.
Coronary vasoconstriction mediated by alpha 1- and alpha 2-adrenoceptors in conscious dogs.
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清醒狗中由α1-和α2-肾上腺素受体介导的冠状血管收缩。
DOI：
10.1152/ajpheart.1987.253.2.h388
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发表时间：
1987
期刊：
影响因子：
--
通讯作者：
Vatner,SF
中科院分区：
文献类型：
--
作者：
Woodman,OL;Vatner,SF
在长期使用仪器的清醒狗中，检查了对α1-和α2-肾上腺素受体选择性刺激的冠状血管收缩反应。去甲肾上腺素（NE，0.05 和 0.1 微克 X kg-1 X min-1），一种混合 α1- 至 α2-肾上腺素受体激动剂，去氧肾上腺素（PE，0.5 和 1.0 微克 X kg-1 X min-1），一种优先 α1-肾上腺素受体激动剂，以及 B-HT 920（1.0 微克 X kg-1 X min-1），一种优先的α2-肾上腺素受体激动剂，在神经节（六甲铵，30 mg/kg iv）、β-肾上腺素受体（普萘洛尔，1.0 mg/kg iv）和毒蕈碱受体（阿托品溴化物，0.1 mg/kg iv）拮抗后静脉输注。 α-肾上腺素受体激动剂的等压剂量导致计算出的舒张末期冠状动脉阻力类似增加（NE，0.57 +/- 0.10 mmHg X ml-1 X min；PE，0.61 +/- 0.13 mmHg X ml-1 X min；B-HT 920，0.64 +/- 0.09 mmHg X ml-1 X min）。以机械方式将主动脉根部压力增加至与α-肾上腺素受体刺激反应中观察到的水平相似的水平并不会增加冠状动脉阻力。哌唑嗪（1 mg/kg iv）优先拮抗α1-肾上腺素受体，消除了对PE的血管收缩反应，但对B-HT 920的反应影响较小。用rauwolscine（α-育亨宾，0.1 mg/kg iv）拮抗α2-肾上腺素受体，消除了对B-HT的血管收缩反应920 但对 PE 反应的影响较小。 α1-或α2-肾上腺素受体拮抗作用可将 NE 的反应降低到类似程度。（摘要截断为 250 字）
Coronary vasoconstriction was examined in response to the selective stimulation of alpha 1- and alpha 2-adrenoceptors in chronically instrumented conscious dogs. Norepinephrine (NE, 0.05 and 0.1 micrograms X kg-1 X min-1), a mixed alpha 1- to alpha 2-adrenoceptor agonist, phenylephrine (PE, 0.5 and 1.0 micrograms X kg-1 X min-1), a preferential alpha 1-adrenoceptor agonist, and B-HT 920 (1.0 micrograms X kg-1 X min-1), a preferential alpha 2-adrenoceptor agonist, were infused intravenously after ganglionic (hexamethonium, 30 mg/kg iv), beta-adrenoceptor (propranolol, 1.0 mg/kg iv), and muscarinic receptor (atropine methylbromide, 0.1 mg/kg iv) antagonism. Equipressor doses of the alpha-adrenoceptor agonists caused similar increases in calculated late diastolic coronary resistance (NE, 0.57 +/- 0.10 mmHg X ml-1 X min; PE, 0.61 +/- 0.13 mmHg X ml-1 X min; B-HT 920, 0.64 +/- 0.09 mmHg X ml-1 X min). Mechanically increasing aortic root pressure to levels similar to those observed in response to alpha-adrenoceptor stimulation did not increase coronary resistance. Preferential antagonism of alpha 1-adrenoceptors with prazosin (1 mg/kg iv) abolished the vasoconstrictor response to PE but had a lesser effect on the response to B-HT 920. Antagonism of alpha 2-adrenoceptors with rauwolscine (alpha-yohimbine, 0.1 mg/kg iv) abolished the vasoconstrictor response to B-HT 920 but had a lesser effect on the response to PE. The response to NE was reduced to a similar degree by either alpha 1- or alpha 2-adrenoceptor antagonism.(ABSTRACT TRUNCATED AT 250 WORDS)