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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。
This work in vitro and in general conditions more easily stroke-induced spontaneous hypertension (SHRSP) and WKY rat vascular α_1 receptor two subtypes. Preincubation of isolated perfused aorta, renal artery and mesenteric artery with 50μmol / L CCl 4 for 30min reduced the maximum contractile tension induced by α_1 receptor in SHRSP and WKY rats to 31.4 ± 8.3% and 35.2 ± 2.9%, 68.4 ± 8.2% and 80.1 ± 7.3%, 68.4 ± 6.3% and 55.4 ± 7.0% of the control, respectively, with no significant difference between the two. However, the blocking effect of 10μmol / L nifedipine on α_1 receptor contractility was significantly higher than that of WKY rats in SHRSP rats (3.1 ± 1.5% and 56.5 ± 4.8%, respectively, P <0.01 ), 9.0 ± 4.1% and 23.6 ± 3.5% (P <0.05), 5.9 ± 2.5% and 28.0 ± 0.8%, respectively (P <0.01). The overall animal experiments also showed that nifedipine antihypertensive effect and the effect on the hypotensive effect of phenylephrine were significantly increased in SHRSP rats compared with WKY rats. The rapid phase and sustained phase contraction induced by α 1 receptor in aorta were mainly caused by the activation of α 1B subtypes. The blocking effect of nifedipine on rapid phase contraction was not significantly different between SHRSP and WKY rats. However, the blocking effect on sustained phase contraction was significantly stronger in SHRSP rats than in WKY rats. The above results suggest that there is no significant change in the distribution of the two subtypes of vascular alpha 1 receptors in SHRSP rats. However, the pathway of secondary extracellular Ca ~ (2 +) entry upon α 1 (1B) agonism is determined by non-dihydropyridine sensitivity Calcium channel into dihydropyridine sensitive calcium channel.