Feres T, Borges A C, Silva E G, Paiva A C, Paiva T B
Department of Biophysics, Escola Paulista de Medicina, São Paulo, SP Brazil.
Br J Pharmacol. 1998 Nov;125(6):1144-9. doi: 10.1038/sj.bjp.0702177.
The alpha2-adrenoceptor function in mesenteric arteries of spontaneously hypertensive rats (SHR) was investigated by comparing membrane potential changes in response to adrenergic agonists in preparations from female SHR, Wistar-Kyoto (WKY) and normotensive Wistar rats (NWR). Resting membrane potential was found to be less negative in mesenteric arteries from SHR than in those from NWR and WKY. Apamin induced a decrease in the membrane potential of mesenteric artery rings without endothelium from NWR and WKY, but had no effects in those from SHR. Both UK 14,304 and adrenaline, in the presence of prazosin, induced a hyperpolarization that was significantly lower in de-endothelialized mesenteric rings from SHR than in those from NWR and WKY. In mesenteric rings with endothelium, however, similar hyperpolarization was observed in the three strains. In NWR mesenteric rings with endothelium the hyperpolarization induced by activation of alpha2-adrenoceptors was abolished by apamin, whereas in intact SHR mesenteric rings this hyperpolarization was slightly reduced by apamin and more efficiently reduced by Nomega-nitro-L-arginine. It is concluded that the activity of potassium channels coupled to alpha2-adrenoceptors is altered in the smooth muscle cells of SHR mesenteric arteries, contributing to their less negative membrane potential. On the other hand, the endothelial alpha2-receptors are functioning in mesenteric vessels from SHR and their stimulation induces a hyperpolarization mainly through the release of nitric oxide.
通过比较雌性自发性高血压大鼠（SHR）、Wistar-Kyoto（WKY）大鼠和正常血压的Wistar大鼠（NWR）肠系膜动脉制剂中肾上腺素能激动剂引起的膜电位变化，研究了SHR肠系膜动脉中的α2-肾上腺素能受体功能。发现SHR肠系膜动脉的静息膜电位比NWR和WKY的更不呈负性。蜂毒明肽可使NWR和WKY无内皮的肠系膜动脉环膜电位降低，但对SHR的肠系膜动脉环无作用。在哌唑嗪存在的情况下，UK 14,304和肾上腺素均诱导超极化，SHR去内皮的肠系膜环中的超极化明显低于NWR和WKY的。然而，在有内皮的肠系膜环中，在这三个品系中观察到类似的超极化。在有内皮的NWR肠系膜环中，α2-肾上腺素能受体激活诱导的超极化被蜂毒明肽消除，而在完整的SHR肠系膜环中，这种超极化被蜂毒明肽轻微降低，被Nω-硝基-L-精氨酸更有效地降低。得出结论，与α2-肾上腺素能受体偶联的钾通道活性在SHR肠系膜动脉平滑肌细胞中发生改变，导致其膜电位更不呈负性。另一方面，内皮α2-受体在SHR的肠系膜血管中发挥作用，其刺激主要通过一氧化氮的释放诱导超极化。
