Neild T O, Kotecha N
Department of Physiology, Monash University, Clayton, Victoria, Australia.
Microvasc Res. 1989 Sep;38(2):186-99. doi: 10.1016/0026-2862(89)90027-7.
Arterioles of the guinea pig small intestine constricted in response to norepinephrine, but the constriction was not maintained. The duration of constriction was reduced after pretreatment by theophylline, 3-isobutyl-1-methyl-xanthine, bromo-cAMP, or bromo-cGMP, suggesting that the relaxation was related to an increase in cyclic nucleotide levels in the cell. Forskolin also reduced the duration of constriction, suggesting the involvement of cAMP. The duration of constriction was not affected by propranolol or isoprenaline, indicating no involvement of beta adrenoceptors. A scheme to explain these observations, in which alpha 1-adrenoceptor activation stimulates adenylate cyclase, leading to a rise in cAMP and an increased rate of intracellular calcium sequestration is proposed. The resulting fall in intracellular calcium leads to repolarization and relaxation.
豚鼠小肠的小动脉对去甲肾上腺素产生收缩反应，但这种收缩并未持续。在用茶碱、3 - 异丁基 - 1 - 甲基黄嘌呤、溴化环磷腺苷（bromo - cAMP）或溴化环磷鸟苷（bromo - cGMP）预处理后，收缩持续时间缩短，这表明松弛与细胞内环核苷酸水平的升高有关。福斯高林也缩短了收缩持续时间，提示环磷腺苷（cAMP）参与其中。收缩持续时间不受普萘洛尔或异丙肾上腺素的影响，表明β肾上腺素能受体未参与。提出了一个解释这些观察结果的方案，即α1 - 肾上腺素能受体激活刺激腺苷酸环化酶，导致环磷腺苷（cAMP）升高和细胞内钙螯合速率增加。细胞内钙的下降导致复极化和松弛。
