大鼠延髓腹面升压区对肾血管紧张性支配及其与α_2受体的关系

Effect of Pressor Area of Ventral Surface of Medulla Oblongata on Renal Vasotonicity and Its Relationship to α_2-Adrenergic Receptor

应用电脉冲或L-谷氨酸局部作用于大鼠延髓腹面升压区(VSM_p),在升压反应的同时,肾交感神经电活动和肾血管阻抗增加,该阻抗的增加依赖于肾神经的完整性。非特异性α受体阻断剂酚妥拉明和特异性α_2受体阻断剂育亨宾阻断肾血管阻抗增加的反应,特异性α_1受体阻断剂哌唑嗪对其无明显影响。结果提示α_2肾上腺素能受体是肾神经传导VSM_P对肾血管紧张性影响的介导因素。

Experiments were performed on 28 urethane--anesthetized Wistar rats. The arterial pressure (AP), renal sympathetic nerve activity (RSNA) and perfusion pressure of kidney (PPk) were recorded. The results showed that: (1) The responses to VSM_p stimulation displayed an enhancement pattern of RSNA, AP and PPl. The PPk effect depended on the existence of intact renal sympathetic nerve (RSN). After RSN was demaged, the PPk did not change anymore during VSM_p stimulation enhancing the RSNA, (2)α-receptor antagonist regitine and α_2-receptor antagonist yohimbine blocked the PPk effect of VSM_p stimulation, but α_1-receptor antagonist prazosin did not alter PPk effect. The results indicated that the PPk effect of VSM_p stimulation was conducted by RSN and mediated by α_2-receptors of renal vessels.