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
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