CALCIUM-ENTRY AND MYOGENIC PHENOMENA IN SKELETAL-MUSCLE ARTERIOLES
CALCIUM-ENTRY AND MYOGENIC PHENOMENA IN SKELETAL-MUSCLE ARTERIOLES
复制标题
DOI：
10.1152/ajpheart.1994.267.3.h1085
复制
发表时间：
1994-09-01
影响因子：
--
通讯作者：
MEININGER, GA
中科院分区：
文献类型：
--
作者：
HILL, MA;MEININGER, GA
研究人员进行了一些研究，以检查与小动脉生肌特性（基础张力、血管舒缩和对血管内压力变化的反应性）相关的几种血管舒缩情况下的 Ca2+ 进入情况。对麻醉大鼠的提睾肌小动脉进行了体内研究。使用压力箱技术增加血管内压力。电压驱动的 Ca2+ 通道 (VOC) 活性被硝苯地平或甲氧基维拉帕米抑制，并被 BAY K 8644 刺激。为了检查超极化的影响，在吡那地尔存在的情况下进行了研究。硝苯地平和甲氧基维拉帕米表现出剂量依赖性扩张趋势；然而，这两种药物都没有引起与腺苷 (10(-4) M) 相当的扩张作用。 BAY K 8644 产生双相效应，在低于 10(-8) M 时收缩，在更高水平时扩张。这些数据表明，基础色调可以通过作用于 VOC 的试剂来调节；然而，由于高浓度的硝苯地平并不能消除音调，因此其他机制也起作用。在相似的浓度下，Ca2+通道拮抗剂显着抑制血管舒缩，在浓度高于 5 x 10(-6) M 时消除血管舒缩。相反，BAY K 8644 引起血管舒缩幅度的剂量依赖性增加（例如，在 10(-7) M 时为基础值的 269 +/- 52%）。因此，血管舒缩似乎高度依赖于挥发性有机化合物。在拮抗剂/激动剂存在下进行的实验表明，VOC 并不是缩窄血管对血管内压力急剧增加的反应的主要决定因素。暴露于吡那地尔会导致剂量依赖性血管舒张和血管舒缩抑制，同时对急性肌源性反应几乎没有影响。在分离的、插管的提睾小动脉中观察到了吡那地尔的类似作用。总的来说，这些数据表明不同的 Ca2+ 进入机制是小动脉基础张力、自发血管舒缩和对血管内压力急剧增加的反应的基础。
Studies were conducted to examine Ca2+ entry in several vasomotor situations related to myogenic properties of arterioles (basal tone, vasomotion, and responsiveness to alterations in intravascular pressure). In vivo studies were performed on small cremaster muscle arterioles of anesthetized rats. Intravascular pressure was increased using the pressure-box technique. Voltage-operated Ca2+ channel (VOC) activity was inhibited by nifedipine or methoxyverapamil and was stimulated with BAY K 8644. To examine the effect of hyperpolarization, studies were performed in the presence of pinacidil. Nifedipine and methoxyverapamil exhibited a trend toward dose-dependent dilation; however, neither agent caused dilation comparable to adenosine (10(-4) M). BAY K 8644 produced a biphasic effect, constriction below 10(-8) M, and dilation at higher levels. These data indicate that basal tone can be modulated by agents acting on VOCs; however, as high concentrations of nifedipine do not abolish tone, other mechanisms contribute. At similar concentrations, the Ca2+ channel antagonist significantly inhibited vasomotion, abolishing vasomotion at concentrations above 5 x 10(-6) M. In contrast, BAY K 8644 caused a dose-dependent increase in vasomotion amplitude (e.g., 269 +/- 52% of basal at 10(-7) M). Thus vasomotion appears highly dependent on VOCs. Experiments per formed in the presence of the antagonists/agonists indicated that VOCs are not the prime determinant of constrictor responses to acute increases in intravascular pressure. Exposure to pinacidil resulted in dose-dependent vasodilatation and inhibition of vasomotion while showing little effect on acute myogenic responses. Similar effects of pinacidil were observed in isolated, cannulated, cremaster arterioles. Collectively, these data suggest that different Ca2+ entry mechanisms underlie arteriolar basal tone, spontaneous vasomotion, and responsiveness to acute increases in intravascular pressure.