Mechanism of adenosine receptor-induced renal vasoconstriction in rats.
Mechanism of adenosine receptor-induced renal vasoconstriction in rats.
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腺苷受体诱导大鼠肾血管收缩的机制。
DOI：
10.1152/ajpheart.1988.255.4.h885
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Amore,B
中科院分区：
文献类型：
--
作者：
Rossi,N;Churchill,P;Ellis,V;Amore,B
腺苷受体A1亚类的选择性腺苷类似物，如n6 -环己基腺苷（CHA），在恒流灌注下诱导离体大鼠肾脏血管收缩。据推测，血管收缩是由肾血管平滑肌细胞中Ca2+浓度增加介导的，但A1腺苷受体占据导致Ca2+增加的机制尚不清楚。在本实验中，分离的、灌注的大鼠肾血管在CHA、K去极化和BAY K 8644（一种Ca2+通道激动剂）的作用下收缩。所有这些反应都被甲氧基维拉帕米完全阻断，这表明CHA，像K去极化和BAY K 8644一样，通过电位操作的Ca2+通道增加Ca2+内流，诱导肾血管收缩。然而，CHA的作用机制不同，百日咳毒素处理阻断了CHA的反应，而不影响对K去极化或BAY K 8644的反应。因此，百日咳毒素敏感的步骤必须干预肾血管平滑肌细胞上A1腺苷受体的占领和通过电位操作的Ca2+通道增加的Ca2+内流。
Adenosine analogues selective for the A1 subclass of adenosine receptors, such as N6-cyclohexyladenosine (CHA), induce vasoconstriction in the isolated rat kidney perfused at constant flow. Presumably, the vasoconstriction is mediated by increased Ca2+ concentration in renal vascular smooth muscle cells, but the mechanism by which A1 adenosine receptor occupation leads to increased Ca2+ is unknown. In the present experiments, the isolated, perfused rat kidney vasoconstricted in response to CHA, to K depolarization, and to BAY K 8644 (a Ca2+ channel agonist). All of these responses were completely blocked by methoxyverapamil, which suggests that CHA, like K depolarization and BAY K 8644, induces renal vasoconstriction by increasing Ca2+ influx through potential operated Ca2+ channels. The mechanism of action of CHA was different, however, in that pertussis toxin treatment blocked the response to CHA without affecting the responses to K depolarization or to BAY K 8644. Therefore, a pertussis toxin-sensitive step must intervene between occupation of A1 adenosine receptors on renal vascular smooth muscle cells and increased Ca2+ influx through potential-operated Ca2+ channels.