自发性高血压大鼠血管α1肾上腺素受体亚型的改变

本工作在离体与整体条件下比较易卒中型自发性高血压(SHRSP)大鼠与WKY大鼠血管中α_1受体的两种亚型。在离体灌流的主动脉、肾动脉与肠系膜动脉,50μmol/L氯甲基可乐定(CEC)预温育30min可使α_1受体激动时引起的最大收缩张力在SHRSP与WKY大鼠分别降为对照时的31.4±8.3％与35.2±2.9％,68.4±8.2％与80.1±7.3％,68.4±6.3％与55.4±7.0％,两者间均无显著性差别。但10μmol/L硝苯吡啶对α_1受体收缩效应的阻断作用则在SHRSP大鼠大大超过WKY大鼠,最大收缩张力分别降为对照时的3.1±1.5％与56.5±4.8％(P<0.01),9.0±4.1％与23.6±3.5％(P<0.05),5.9±2.5％与28.0±0.8％(P<0.01)。整体动物实验也显示硝苯吡啶的降血压作用及对苯肾上腺素升血压效应的阻断作用在SHRSP大鼠都较WKY大鼠显著增强。离体主动脉a_1受体激动时的快速相与持续相收缩均主要由α_(1B)亚型激动引起,硝苯吡啶对快速相收缩的阻断作用在SHRSP与WKY大鼠无显著性差别,但对持续相收缩的阻断作用则在SHRSP大鼠显著强于WKY大鼠。上述结果提示SHRSP大鼠血管α_1受体两种亚型的分布没有显著改变,但α_(1B)受体激动时继发性细胞外Ca~(2+)进入的途径由非双氢吡啶敏感性钙通道转变为双氢吡啶敏感性钙通道。

Changes of subtypes of alpha 1-adrenoceptor in blood vessels of spontaneously hypertensive rats]

The two subtypes of alpha 1-adrenoceptors in blood vessels were compared between stroke prone spontaneously hypertensive rats (SHRSP) and WKY rats in vitro and in vivo. Pretreatment with 50 mumol/L chlorethylclonidine (CEC) for 30 min decreased the maximal contractions induced by norepinephrine (NE) to 31.4 +/- 8.3% and 35.2 +/- 2.9% (aortae); 68.4 +/- 8.2% and 80.1 +/- 7.2% (renal arteries); 68.4 +/- 6.3% and 5.4 +/- 7.0% (mesenteric arteries) of the controls in the SHRSP and the WKY rats, respectively. All the differences between the SHRSP and WKY rats were not statistically significant. In contrast, the blocking effects of nifedipine were much stronger in the SHRSP rats than those in the WKY rats. In the presence of 10 mumol/L nifedipine the maximal contractions induced by NE were decreased to 3.1 +/- 1.5% and 56.5 +/- 4.8% (P < 0.01, aortae); 9.0 +/- 4.1% and 23.6 +/- 3.5% (P < 0.05, renal arteries); 5.9 +/- 2.5% and 28.0 +/- 0.8% (P < 0.01, mesenteric arteries) of the controls in the SHRSP and the WKY rats, respectively. The experiment in vivo also showed that the effects of nifedipine on decreasing basal blood pressure and on antagonizing phenylephrine were increased in the SHRSP rats, as compared to the WKY rats. Analyses of two components of the contractions induced by 10 mumol/L NE in aortae demonstrated that both phasic and tonic contractions were mainly caused by activations of the alpha 1B subtype. There were no significant differences of blocking effects of nifedipine on the phasic contractions between the SHRSP and WKY rats.(ABSTRACT TRUNCATED AT 250 WORDS)