大鼠主动脉α_1肾上腺素能受体激活引起Ca^（2＋）内流的特性

Character of the Ca￣(2+) entry induced by activation of α_1-adrenoceptor in rat aorta

在大鼠主动脉平滑肌标本上，０．５μｍｏｌ．Ｌ－１硝苯吡啶能完全阻断由１００ｍｍｏｌ·Ｌ－１ＫＣｌ引起的血管收缩和４５Ｃａ内流；并部分抑制苯肾上腺素引起的血管收缩效应和４５Ｃａ内流；６ｍｍｏｌ·Ｌ－１普鲁卡因能完全阻断无钙Ｋｒｅｂｓ液中苯肾上腺素引起的血管收缩和４５Ｃａ外溢，且部分阻断正常Ｋｒｅｂｓ液中苯肾上腺素引起的血管收缩和４５Ｃａ内流；０．５μｍｏｌ·Ｌ－１硝苯吡啶和６ｍｍｏｌ·Ｌ－１普鲁卡因合用能阻断苯肾上腺素引起的Ｃａ２＋内流。提示：α１受体兴奋后引起的细胞外Ｃａ２＋内流可分为硝苯吡啶敏感和不敏感两部分，而后者受细胞内Ｃａ２＋释放调节。

In rat aorta, 0.5μmol. L-1nifedipine(Nif) completely blocked the contractile response and 45Ca influx induced by 100mmol. L-1 KCl and partially inhibited phenylephrine(PHE) -induced contractile response and 45Ca influx. 6 mmol. L-1 procaine competely blocked the contractile response and 45Ca efflux in Ca2+ free Krebs solution and partially inhibited contractile response and 45Ca influx in normal krebs solution induced by PHE. 0.5μmol. L-1 Nif plus 6 mmol. L-1 procaine completely blocked PHE-induced Ca2+ entry. These results suggest that the extracellular Ca2+ entry induced by activation of α1-adrenoceptor contains two components, sensitive to Nif and insensitive to Nif; The latter is partially regulated by intracel lular Ca2+ release.