Control of renal hemodynamics- with special reference on isolated afferent arteriole

肾循环主要由传入小动脉和传出小动脉两条阻力血管调节。许多实验结果表明，每个小动脉对各种生理刺激和血管活性物质具有不同的敏感性。因此，为了了解肾血流动力学的调节机制，了解传入和传出小动脉对血管活性物质的敏感性是否不同是非常重要的。血管紧张素II(Ang II)和精氨酸加压素(AVP)是一种强大的血管收缩药，它们在调节肾脏血流动力学方面发挥着重要作用。因此，在本研究中，我们在体外和活体条件下观察了Ang II和AVP对传入小动脉的影响，特别是内皮源性松弛因子(EDRF)-一氧化氮(NO)。1)体外实验：从新西兰大白兔肾脏显微解剖浅传入小动脉。每个传入动脉…用微量吸管系统插入更多的LE，腔内压力设定为60毫米汞柱。我们发现去甲肾上腺素以剂量依赖的方式减小传入小动脉的管腔直径，但Ang II即使在高剂量(10^&lt；-6&gt；M)也不影响管腔直径。但给予一氧化氮合酶抑制剂L-NNA后，Ang II呈剂量依赖性收缩传入小动脉(10^&lt；-12&gt；-10&gt；M)。(2)体内实验：在戊巴比妥钠麻醉的犬，血管加压素V2受体的兴奋是否引起肾血管扩张，NO是否参与此过程。肾内注射AVP可引起肾血管收缩。然而，在V1拮抗剂预处理后，AVP引起显著的血管扩张。经V2拮抗剂治疗后，这种血管扩张作用消失。即使在没有V2受体拮抗剂的情况下，肾内注射L-NA也能减弱血管的扩张。这些结果清楚地表明，肾血管的扩张是由V2受体介导的。NO可能参与了这种肾血管扩张。较少

Renal circulation is mainly regulated by two resistance vessels, the afferent arteriole and the efferent arteriole. Many experimental findings show that each arteriole has a different sensitivity to various kinds of physiological stimuli and vasoactive substances. Thus, for understanding the regulatory mechanisms of renal hemodynamics, it is very important to know whether or not sensitivity to vasoactive substances is different between the afferent and efferent arteriole. Angiotensin II(Ang II) and arginine vasopressin (AVP) are potent vasoconstrictors and they exert an important role to the regulation of renal hemodynamics. So, in the present study, we examined the effects of Ang II and AVP on the afferent arteriole in both in vitro and in vivo conditions, with special reference to endothelium derived relaxing factor(EDRF)-nitric oxide(NO).1) in vitro experiment : The superficial afferent arterioles were microdissected from the kidney of New Zealand White rabbit. Each afferent arterio … More le was cannulate with a micropipette system, and the intraluminal pressure was set at 60 mmHg. We found that norepinephrine decreased the lumen diameter of the afferent arteriole in a dose-dependent manner, but Ang II even at high dose(10^<-6>M) did not affect the lumen diameter. However, after the pretreatment of L-NNA which is an inhibitor of NO synthase, Ang II constricted the afferent arteriole in a dose-dependent manner(10^<-12> - 10^<-10>M). AVP(10^<-6>M) slightly decreased the diameter, but the constrictor action of AVP was markedly enhanced by L-NNA.2) in vivo experiment : Using pentobarbital -anesthetized dogs, we investigated whether or not vasopressin V2-receptor stimulation induced renal vasodilation and whether NO had a role in the process. Intrarenal infusion of AVP resulted in renal vasoconstriction. However, following pretreatment of a V1-antagonist, AVP caused a significant vasodilation. This vasodilation disappeared after the treatment of V2-antagonist. Even in the absence of the V2-antagonist, vasodilation was attenuated by intrarenal infusion of L-NNA.These findings clearly indicate that renal vasodilation is mediated by the V2 receptors. NO may participate in this renal vasodilation. Less