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

肾循环主要由两条阻力血管调节，即输入小动脉和输出小动脉。许多实验结果表明，每个微动脉对各种生理刺激和血管活性物质的敏感性不同。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（Angiotensin II，Ang II）和精氨酸加压素（arginine vasopressin，AVP）是强效的血管收缩剂，对肾脏血流动力学的调节发挥重要作用。因此，本研究在体外和体内条件下观察了血管紧张素Ⅱ和精氨酸加压素对传入小动脉的作用，特别是内皮源性舒张因子（EDRF）-一氧化氮（NO）。1）体外实验：从新西兰白色兔肾脏显微解剖浅传入小动脉。每根传入动脉 ...更多信息 用微量移液管系统对le进行插管，并将管腔内压力设定为60 mmHg。我们发现去甲肾上腺素以剂量依赖性方式减小传入小动脉的管腔直径，但Ang II即使在高剂量（10 μ <-6>M）下也不影响管腔直径。然而，在NO合成酶抑制剂L-NNA预处理后，Ang II以剂量依赖性方式（10 μ M<-12>- 10 μ <-10>M）收缩传入小动脉。AVP（10 μ <-6>M）使肾血管直径略有减小，但L-NNA可明显增强AVP的收缩作用。2）体内实验：用戊巴比妥麻醉的狗，研究加压素V_2受体激动是否引起肾血管舒张以及NO在此过程中是否起作用。肾内注射AVP可引起肾血管收缩。然而，预处理后的V1-拮抗剂，AVP引起了显着的血管舒张。V2受体拮抗剂治疗后血管舒张消失。即使在没有V2受体拮抗剂的情况下，肾内注射L-NNA也能减弱血管舒张作用，这些结果清楚地表明肾血管舒张是由V2受体介导的。NO可能参与了这种肾血管舒张作用。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