Miasiro N, Paiva A C
Department of Biophysics, Escola Paulista de Medicina, Sao Paulo, Brazil.
Eur J Pharmacol. 1990 Apr 10;179(1-2):151-8. doi: 10.1016/0014-2999(90)90412-y.
The effects of endothelin-1 on normal and everted rabbit aorta rings and on cultured rat aortic smooth muscle cells were studied. Endothelin-1 (40 nM) contracted both normal and everted rings, and was still able to induce a prolonged contraction in Ca2(+)-free medium. Treatment of cultured cells with 100 nM endothelin-1 caused a sharp transient increase in 45Ca2+ efflux. The contractile and 45Ca2+ responses showed severe and specific desensitization towards endothelin-1; the responses to angiotensin II and adrenaline were not affected. The contractile responses to endothelin-1 were not affected by previous treatment with angiotensin II or with the angiotensin receptor antagonist, [Sar1,Ala8]angiotensin II. It is concluded that endothelin-1 acts on its own specific receptors to elicit Ca2+ mobilization from both intracellular and extracellular sources.
研究了内皮素-1对正常和外翻兔主动脉环以及培养的大鼠主动脉平滑肌细胞的影响。内皮素-1（40 nM）使正常和外翻环均收缩，并且在无Ca2+的培养基中仍能够诱导长时间收缩。用100 nM内皮素-1处理培养的细胞导致45Ca2+外流急剧短暂增加。收缩和45Ca2+反应对内皮素-1表现出严重且特异性的脱敏；对血管紧张素II和肾上腺素的反应未受影响。内皮素-1的收缩反应不受预先用血管紧张素II或血管紧张素受体拮抗剂[Sar1,Ala8]血管紧张素II处理的影响。结论是内皮素-1作用于其自身特异性受体以引发细胞内和细胞外来源的Ca2+动员。
