Pulmonary vasoreactivity to serotonin during hypoxia is modulated by ATP-sensitive potassium channels.

Pulmonary vasoreactivity to serotonin during hypoxia is modulated by ATP-sensitive potassium channels.
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缺氧期间肺血管对血清素的反应性受到 ATP 敏感钾通道的调节。

DOI:
10.1152/jappl.1997.83.2.569
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发表时间:
1997
期刊:
Journal of applied physiology (Bethesda, Md. : 1985)
影响因子:
--
通讯作者:
Barman,SA
Barman,SA
中科院分区:
--
文献类型:
--
作者:
Barman,SA

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缺氧期间肺血管对血清素的反应性由 ATP 敏感钾通道调节。应用。 Physiol.83(2): 569–574, 1997.—在离体血液灌注狗肺中确定缺氧期间 ATP 敏感 K+ 通道调节在犬肺血管对血清素反应中的作用。使用血管闭塞技术测量肺血管阻力和顺应性。在常氧条件下,血清素 (10−5M) 显着增加毛细血管前和毛细血管后阻力以及肺毛细血管压力,并通过降低微血管和大血管顺应性来降低总血管顺应性。在缺氧期间,血清素对毛细血管前和毛细血管后阻力、毛细血管压力以及微血管顺应性和大血管顺应性的影响增强。在常氧条件下,ATP敏感的K+通道开放剂cromakalim (10−5M)抑制对毛细血管后阻力和微血管顺应性的血清素反应,而在缺氧条件下,cromakalim抑制血清素对毛细血管前和毛细血管后阻力、毛细血管压力以及微血管和大血管顺应性的增强作用。这些结果表明,犬肺血管对血清素的反应性在缺氧条件下增强,并且 ATP 敏感的 K+通道调节对血清素的升压反应,这种作用在缺氧期间更为明显。
Barman, Scott A.Pulmonary vasoreactivity to serotonin during hypoxia is modulated by ATP-sensitive potassium channels.J. Appl. Physiol.83(2): 569–574, 1997.—The role of ATP-sensitive K+-channel modulation in the canine pulmonary vascular response to serotonin during hypoxia was determined in the isolated blood-perfused dog lung. Pulmonary vascular resistances and compliances were measured by using vascular occlusion techniques. Under normoxia, serotonin (10−5M) significantly increased precapillary and postcapillary resistances and pulmonary capillary pressure and decreased total vascular compliance by decreasing both microvascular and large-vessel compliances. During hypoxia, the effect of serotonin was potentiated on both precapillary and postcapillary resistance and capillary pressure, as well as on microvascular compliance and large-vessel compliance. Under normoxia, the ATP-sensitive K+-channel opener cromakalim (10−5M) inhibited the serotonergic response on postcapillary resistance and microvascular compliance, whereas during hypoxia cromakalim inhibited the potentiated effect of serotonin on both precapillary and postcapillary resistance, capillary pressure, and both microvascular and large-vessel compliances. These results indicate that canine pulmonary vasoreactivity to serotonin is heightened under hypoxic conditions and that ATP-sensitive K+channels modulate the pressor response to serotonin, an effect that is more pronounced during hypoxia.
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