INSITU ANALYSIS OF ALPHA-ADRENOCEPTORS ON ARTERIOLAR AND VENULAR SMOOTH-MUSCLE IN RAT SKELETAL-MUSCLE MICROCIRCULATION
INSITU ANALYSIS OF ALPHA-ADRENOCEPTORS ON ARTERIOLAR AND VENULAR SMOOTH-MUSCLE IN RAT SKELETAL-MUSCLE MICROCIRCULATION
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DOI：
10.1161/01.res.62.1.37
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发表时间：
1988-01-01
影响因子：
20.1
通讯作者：
FABER, JE
中科院分区：
文献类型：
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作者：
FABER, JE
本研究的目的是确定在微血管的血管平滑肌上是否存在α 1-和α 2-肾上腺素能受体，以及解剖学上不同的微血管节段的肾上腺素能收缩是否由任一受体亚型不同地辅助。将麻醉大鼠的提睾肌骨骼肌急性去神经支配并悬浮在含有可卡因、去甲肾上腺素和普萘洛尔的Krebs浴中以阻断摄取1、摄取2和β-肾上腺素。受体，分别。活体显微镜用于研究大的分布小动脉（平均直径，100 μ m）、小的毛细血管前小动脉（25 μ m）和电容小静脉（140 μ m）。在不存在或存在拮抗剂哌唑嗪（α 1）和育亨宾（α 2）的情况下，获得浴中加入的激动剂去甲肾上腺素（混合α 1/α 2）、苯肾上腺素（α 1）和B-HT 933（α 2）的浓度-反应（直径变化）曲线。大动脉和小静脉的表观pD 2（-log ED 50）值分别如下：去甲肾上腺素（7.41和7.15）、苯肾上腺素（5.95和5.41）和B-HT 933（5.05和5.06）。低浓度的哌唑嗪（10-8 M）和育亨宾（10-7 M）产生受体亚型选择性拮抗作用和大动脉和小静脉的去甲肾上腺素曲线的平行，右旋位移。大动脉pKB（-log KB）为7.83 ±。0.65哌唑嗪和7.36 ±。0.46育亨宾较高浓度的哌唑嗪（10-7和3 × 10 - 6）可用于治疗。10-7 M）和育亨宾（10-6 M）使去甲肾上腺素曲线进一步右旋但非平行位移。相比之下，受体亚型选择性浓度的育亨宾抑制肾上腺素能收缩的小，毛细血管前的小动脉，但哌唑嗪在受体亚型选择性浓度没有影响。这些数据表明，骨骼肌中大的小动脉和小静脉的肾上腺素能调节使用α 1-和α 2-肾上腺素受体。然而，毛细血管前小动脉可能主要受α 2受体的影响。
The purpose of this study was to determine whether both .alpha.1- and .alpha.2-adrenergic receptors exist on vascular smooth muscle of microvessels and whether adrenergic constriction of anatomically distinct microvascular segments is differentially subserved by either receptor subtype. The cremaster skeletal muscle of anesthetized rats was acutely denervated and suspended in a Krebs bath containing cocaine, normetanephrine, and propranolol to block uptake1, uptake2, and .beta.-receptors, respectively. Intravital microscopy was used to study large distributing arterioles (mean diameter, 100 .mu.m), small precapillary arterioles (25 .mu.m), and capacitance venules (140 .mu.m). Concentration-response (diameter change) curves were obtained for bath-added agonists norepinephrine (mixed .alpha.1/.alpha.2), phenylephrine (.alpha.1), and B-HT 933 (.alpha.2) in the absence or presence of antagonists prazosin (.alpha.1) and yohimbine (.alpha.2). Apparent pD2 (-log ED50) values for large arterioles and venules were, respectively, as follows: norepinephrine (7.41 and 7.15), phenylephrine (5.95 and 5.41), and B-HT 933 (5.05 and 5.06). Low concentrations of prazosin (10-8 M) and yohimbine (10-7 M) produced receptor subtype-selective antagonism and parallel, dextral displacement of norepinephrine curves for large arterioles and venules. The large arteriole pKB (-log KB) was 7.83 .+-. 0.65 for prazosin and 7.36 .+-. 0.46 for yohimbine. Higher concentrations of prazosin (10-7 and 3 .times. 10-7 M) and yohimbine (10-6 M) produced further dextral but nonparallel displacement of norepinephrine curves. In contrast, receptor subtype-selective concentrations of only yohimbine inhibited adrenergic constriction of small, precapillary arterioles; but prazosin had no effect at receptor subtype-selective concentrations. These data suggest that adrenergic regulation of large arterioles and venules in skeletal muscle uses both .alpha.1- and .alpha.2-adrenoceptors. Precapillary arterioles, however, may be subserved predominantly by .alpha.2-receptors.