Lai F M, Tanikella T, Thibault L, Chan P S, Cervoni P
J Pharmacol Exp Ther. 1980 Aug;214(2):388-94.
Contractile responses to norepinephrine, serotonin and potassium (K+) and relaxant responses to isoproterenol and papaverine were studied in vitro with spirally cut thoracic aortic strips from aortic coarcted hypertensive rats (AHR)2, 6, 14 and 28 days postoperatively and compared to time-matched, sham-operated normotensive controls. At every stage after coarctation, the rats developed hypertension with elevated plasma renin activity. In response to stimulation by norepinephrine and serotonin, aortic strips from 2 to 28 day AHR developed the same tension as controls, whereas aortas of 6 and 14 day AHR had reduced maximal responses. For K+-stimulated aortic strips, maximal contractile force was decreased at 6 day AHR only. Relaxation by isoproterenol and papaverine in serotonin-contracted aortas was the same in AHR and normotensive controls 2 and 28 days postoperatively but was reduced at 6 and 14 days. The demonstrated changes of vascular contractility and relaxation in AHR is a hypertensive stage-dependent phenomenon. It is speculated that 6 and 14 days after coarctation the diminished relaxant ability of the aortas helps to maintain the elevated blood pressure and the diminished sensitivity to contractile stimulants is a protective mechanism in response to the elevated blood pressure. The return of normal contraction and relaxation to the agonists in the chronic stage of hypertension may possibly reflect an adaptive change to the prolonged stimulus of the elevated blood pressure that aortic tissue had undergone in order to maintain normal physiologic functions.
在体外,使用主动脉缩窄性高血压大鼠(AHR)术后2、6、14和28天的螺旋形切割胸主动脉条,研究了对去甲肾上腺素、5-羟色胺和钾离子(K+)的收缩反应以及对异丙肾上腺素和罂粟碱的舒张反应,并与时间匹配的假手术正常血压对照进行比较。在缩窄后的每个阶段,大鼠均出现高血压且血浆肾素活性升高。对去甲肾上腺素和5-羟色胺刺激的反应,术后2至28天的AHR主动脉条产生的张力与对照相同,而术后6天和14天的AHR主动脉最大反应降低。对于K+刺激的主动脉条,仅术后6天的AHR最大收缩力降低。术后2天和28天,AHR和正常血压对照中,异丙肾上腺素和罂粟碱对5-羟色胺收缩的主动脉的舒张作用相同,但在术后6天和14天降低。AHR中血管收缩性和舒张性的变化是一种高血压阶段依赖性现象。推测缩窄后6天和14天,主动脉舒张能力减弱有助于维持血压升高,而对收缩刺激的敏感性降低是对血压升高的一种保护机制。高血压慢性期对激动剂的收缩和舒张反应恢复正常,可能反映了主动脉组织为维持正常生理功能而对血压升高的长期刺激所发生的适应性变化。