内毒素血症大鼠血管α_1肾上腺素受体及其亚型的改变

CHANGES OF α_1-ADRENOCEPTOR AND ITS SUBTYPES IN BLOOD VESSELS OF ENDOTOXEMIA RATS

内毒素血症大鼠离体主动脉、肾动脉与肠系膜动脉对去甲肾上腺素(NE)的浓度——收缩反应曲线显著右移,最大收缩反应显著降低,CEC对上述反应的影响不变,但硝苯吡啶的抑制作用显著增强,这种增强在主动脉只表现在持续相收缩中,而对快速相收缩的影响不变。NE对内毒素血症大鼠主动脉磷酸肌醇生成的刺激作用以及CEC与硝苯吡啶对上述作用的影响均与对照无显著差别。结果提示内毒素血症大鼠血管平滑肌上a_1受体的数量、两种亚型(a_(1A)与a_(1B))的比例乃至受体激动后磷酸肌醇的生成都无明显改变,但a_(1B)受体激动后继发性细胞外Ca^(2+)进入的途径由正常时的非双氢吡啶敏感性钙通道转变为双氢吡啶敏感的钙通道。

In aortae, renal arteries and mesenteric arteries isolated from endotoxemia rats, the concentration-contraction response curves for norepinephrine (NE) were shifted to the right and the maximalcontractions induced by NE were reduced significantly. The effect of CEC on NE induced contractionswas not changed, while the inhibition effect of nifedipine was significantly increased. In aortae theenhanced effect of nifedipine was only shown in the tonic contraction but not in the phasic contrac-tion. The formation of inositol phosphates (InsPs) stimulated by NE and the effects of CEC andnifedipine on the InsPs formation were not changed in aortae isolated from endotoxemia rats. Theresults suggest that in smooth muscles of blood vessels isolated from endotoxemia rats the amount ofa_1-adrenoceptor, the distribution of two subtypes of a_1-adrenoceptor, and formation of InsPs stimu-lated by a_1-adrenoceptor are not changed. but the pathway for Ca^(2+) entry followed by mobilizationof intracellular Ca^(2+) turn to be dihydropyridine sensitive chennel instead of non-dihydropyridinesensitive channel as in normal rats.