Huguet F, Brisac A M, Dubar M, Ingrand P, Piriou A
Institut des Xénobiotiques, Faculté de Médecine et de Pharmacie, Poitiers, France.
Int J Dev Neurosci. 1993 Jun;11(3):295-301. doi: 10.1016/0736-5748(93)90001-t.
Previous studies in rats have demonstrated both the link between voltage-operated calcium channels and endothelin and their cerebral involvement in the pathophysiology of spontaneous hypertension. In the present study, the interaction of endothelin with specific dihydropyridine (DHP) binding sites was investigated using the brain slices model. In rat hippocampal slices, pre-incubation with Bay K 8644 decreased [3H] (+) PN 200-110 binding. There was no difference in agonist-induced decrease of DHP binding in normotensive and spontaneously hypertensive (SH) rats. The effect of Bay K 8644 was partially inhibited by endothelin but not by angiotensin in both normotensive and hypertensive rats. These data compared to those of other studies suggest that DHP binding sites which are regulated by endothelin are post-synaptic. We conclude that brain slices provide a good in vitro model to study DHP receptor regulation and to explore endothelin interactions with DHP-sensitive Ca2+ channels.
先前在大鼠身上进行的研究已经证明了电压门控钙通道与内皮素之间的联系,以及它们在自发性高血压病理生理学中的脑内作用。在本研究中,使用脑片模型研究了内皮素与特定二氢吡啶(DHP)结合位点的相互作用。在大鼠海马脑片中,用Bay K 8644预孵育可降低[3H](+)PN 200 - 110的结合。在正常血压和自发性高血压(SH)大鼠中,激动剂诱导的DHP结合减少没有差异。在正常血压和高血压大鼠中,Bay K 8644的作用均被内皮素部分抑制,但不被血管紧张素抑制。与其他研究的数据相比,这些数据表明受内皮素调节的DHP结合位点位于突触后。我们得出结论,脑片为研究DHP受体调节和探索内皮素与DHP敏感Ca2+通道的相互作用提供了一个良好的体外模型。