P物质在家兔延髓腹侧面加压区的升压作用及其机制探讨

PRESSOR EFFECT OF SUBSTANCE P APPLIED TO THE PRESSOR AREA OF VENTRAL SURFACE OF MEDULLA OBLONGATA AND THE UNDERLYING MECHANISM IN RABBITS

在乌拉坦麻醉、三碘季铵酚制动、人工呼吸的家兔上观察到，延髓腹侧面加压区（VSMP）给予P物质（SP）使血压（BP）呈剂量依赖性升高，但对心率无明显影响。VSMP给予SP受体阻断剂使BP明显降低并可阻断SP升压效应。VSMP给予酚妥拉明或哌唑嗪预处理使SP升压效应减弱或消失，而给予育亨宾或心得安对SP升压效应无明显影响。VSMP给予SP可使肾交感神经放电（RSND）显著增加，并伴有BP显著升高；VSMp给予DSP使RSND和BP明显降低并可阻断SP的RSND增加和升压效应。结果表明：SP在VSMP具有升压作用，这是由于激活VSMp的SP受体所致，并有该局部α1受体参与介导。此升压效应主要是通过交感神经活动增强使外周血管阻力增加而实现的。VSMp的内源性SP有参与维持交感缩血管紧张性和BP水平的作用。

Experiments were performed on urethane anesthetized and artificially ventilatedrabbits. The results were as follows. Application of substance P (SP) to the pressorarea of ventral surface of medulla oblongata (VSMp) elicited a dose-dependent increasein blood pressure (BP), but no significant change in heart rate. The pressor response ofSP was blocked by pretreatment with SP receptor antagonist (DSP) in VSMP. Application of DSP alone to VSMp elicited a significant decrease in BP. The pressor responseof SP was attenuated when VSMp was pretreated with phentolamine or prazosine,whereas pretreatment with yohimbin or propranolol was without effect. Application ofSP to VSMp elicited an increase in renal sympathetic nerve discharge (RSND) in association with pressor response; both these responses were blocked by pretreatment withDSP in VSMp. Application of DSP alone to VSMp elicited a significant decrease inRSND and BP. The above results indicate that SP has a pressor effect in VSMp due toactivation of SP receptor mediated by α1-receptor. The pressor effect of SP may bemainly due to an increase of peripheral vascular resistance induced by the augmentedsympathetic nerve activity. In summary, it appears that endogenous SP in VSMp playsan important role in maintaining sympathetic tone and BP level.