Stimulation of adenylate cyclase by adenosine and other agonists in mesenteric artery smooth muscle cells in culture.
Stimulation of adenylate cyclase by adenosine and other agonists in mesenteric artery smooth muscle cells in culture.
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腺苷和其他激动剂对培养的肠系膜动脉平滑肌细胞中腺苷酸环化酶的刺激。
DOI：
10.1016/0024-3205(85)90521-1
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发表时间：
1985
期刊：
影响因子：
6.1
通讯作者：
D. Franks
中科院分区：
文献类型：
--
作者：
M. Anand;D. Franks
在培养的肠系膜动脉平滑肌细胞中发现了一种腺苷敏感腺苷酸环化酶。n -乙基羧酰胺-腺苷（NECA）、n -甲基羧酰胺-腺苷（MECA）、l- n6 -苯异丙基腺苷（PIA）和2-氯腺苷（2-cl-Ado）均以浓度依赖的方式刺激腺苷酸环化酶。NECA是最有效的模拟物（EC50, 1 μM），而PIA (EC50, 15 μM), 2-Cl-Ado （EC50, 15 μM）和MECA （EC50, 24 μM）的效力较弱，相对于NECA的效力分别为0.61,0.61和0.65。腺苷表现出双相效应：低浓度刺激和高浓度抑制，而2 '脱氧腺苷仅抑制腺苷酸环化酶活性。NECA对腺苷酸环化酶的刺激作用依赖于金属离子浓度，并被3-异丁基- 1 -甲基黄嘌呤（IBMX）和8-苯基茶碱（8-PT）阻断。其他激动剂如肾上腺素、去甲肾上腺素、前列腺素、多巴胺、NaF和forskolin也能刺激这些培养细胞的腺苷酸环化酶。异丙肾上腺素、肾上腺素和去甲肾上腺素对腺苷酸环化酶的刺激可被丙萘酚阻断，而酚妥拉明不能。另一方面，酚妥拉明、丙萘酚和氟哌噻醇均抑制多巴胺刺激的腺苷酸环化酶活性。此外，最佳PIA浓度的刺激是加性的或几乎加性的，最大的刺激是catacholamine和前列腺素。这些数据表明，在肠系膜动脉平滑肌细胞中存在腺苷（刺激“Ra”）、儿茶酚胺和前列腺素受体，并提示这些药物可能通过与腺苷酸环化酶偶联的各自受体相互作用来发挥其生理作用。
An adenosine-sensitive adenylate cyclase has been characterized in cultured mesenteric artery smooth muscle cells. N-Ethylcarboxamide-adenosine (NECA), N-Methylcarboxamide-adenosine (MECA), L-N6-phenylisopropyladenosine (PIA) and 2-chloroadenosine (2-cl-Ado) all stimulated adenylate cyclase in a concentration dependent manner. NECA was the most potent analog (EC50, 1 μM), whereas PIA (EC50, 15 μM), 2-Cl-Ado (EC50, 15 μM) and MECA (EC50, 24 μM), were less potent and had efficacies relative to NECA of 0.61, 0.61 and 0.65, respectively. Adenosine showed a biphasic effect: stimulation at lower concentrations and inhibition at higher concentrations, whereas 2′ deoxyadenosine only inhibited adenylate cyclase activity. The stimultory effect of NECA on adenylate cyclase was dependent on metal ion concentration and was blocked by 3-isobutyl-l-methylxanthine (IBMX) and 8-phenyltheophylline (8-PT). Adenylate cyclase from these cultured cells was also stimulated by other agonists such as epinephrine, norepinephrine, prostaglandins, dopamine, NaF and forskolin. The stimulation of adenylate cyclase by isoproterenol, epinephrine and norepinephrine was blocked by propranalol but not by phentolamine. On the other hand, phentolamine, propranalol and flupentixol all inhibited dopamine-stimulated adenylate cyclase activity. In addition, the stimulation by an optimal concentration of PIA was additive or almost additive with maximal stimulation caused by catacholamines and prostaglandins. These data indicate the presence of adenosine (Stimulatory “Ra”), catecholamine and prostaglandin receptors in mesenteric artery smooth muscle cells and suggest that these agents may exert their physiological actions through their interaction with their respective receptors coupled to adenylate cyclase.