In vivo evidence that an adenylate cyclase-cAMP system dilates cerebral arterioles in mice.

In vivo evidence that an adenylate cyclase-cAMP system dilates cerebral arterioles in mice.
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体内证据表明腺苷酸环化酶-cAMP 系统可扩张小鼠的脑小动脉。

DOI:
10.1161/01.str.19.7.888
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发表时间:
1988
期刊:
影响因子:
8.3
通讯作者:
Rosenblum,WI
Rosenblum,WI
中科院分区:
医学1区
文献类型:
--
作者:
Rosenblum,WI

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通过电视显微镜监测用乌拉坦麻醉的活小鼠的软膜小动脉。我测试了腺苷酸环化酶-环磷酸腺苷(cAMP)系统的存在,通过局部应用以下药物扩张小动脉:cAMP(10(-3)M),其更有效的类似物二丁酰cAMP(10(-3)和10(-4)M),和毛喉素(10(-6)M)。毛喉素激活内源性腺苷酸环化酶,导致内源性cAMP增加。每种药物应用30秒;所有三种药物都产生扩张。然后,在存在或不存在10(-4)M异丁基甲基黄嘌呤(IMX)的情况下,我应用cAMP或毛喉素,IMX是一种内源性磷酸二酯酶抑制剂,可破坏cAMP。IMX的存在显着增强了由外源性cAMP和毛喉素产生的扩张。这些数据表明,小鼠的大脑表面小动脉对cAMP的反应是扩张,并含有产生和灭活这种扩张剂的酶。软膜小动脉中腺苷酸环化酶-cAMP扩张机制的存在并不排除其他扩张机制的同时存在。
Pial arterioles of living mice anesthetized with urethane were monitored by television microscopy. I tested the existence of an adenylate cyclase-cyclic adenosine monophosphate (cAMP) system for dilating the arterioles by topically applying the following drugs: cAMP (10(-3) M), its more potent analogue dibutyryl cAMP (10(-3) and 10(-4) M), and forskolin (10(-6) M). Forskolin activates endogenous adenylate cyclase, which leads to increases in endogenous cAMP. Each drug was applied for 30 seconds; all three produced dilation. I then applied either cAMP or forskolin in the presence or absence of 10(-4) M isobutylmethylxanthine (IMX), an inhibitor of endogenous phosphodiesterase, which destroys cAMP. The presence of IMX significantly potentiated the dilation produced by exogenous cAMP and forskolin. These data indicate that cerebral surface arterioles of mice respond to cAMP with dilation and contain the enzymes for producing and inactivating this dilator. The existence of an adenylate cyclase-cAMP dilating mechanism in pial arterioles does not rule out the simultaneous existence of other dilating mechanisms.
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