Control of renal hemodynamics -with special reference to tubulo-glomerular feedback-

尽管灌注压变化很大，但肾血流量保持恒定，这种现象称为自动调节。现在已经确定肾自身调节是由肾小管肾小球反馈（TGF）介导的。TGF是一种负反馈系统，可稳定肾单位血流量、单肾单位肾小球滤过率和肾小管流速。肾灌注压的增加通过GFR的增加而增加肾小管流速，肾小管流速的增加导致致密斑处氯化钠浓度的升高。这被致密斑感觉到，并导致传入小动脉阻力增加。本研究的目的是确定致密斑作为感受细胞向作为效应器官的传入小动脉传递信息的递质。我们已经集中于腺苷和一氧化氮（NO）作为体内实验的可能候选物1）腺苷：transmitter.I.in ...更多信息 在麻醉犬中检查肾血流动力学和间质腺苷水平。肾内输注高渗盐水导致肾血流量（RBF）下降，随后肾血流量（RBF）短暂增加，间质腺苷浓度显着增加。腺苷1受体拮抗剂可完全阻断高渗盐水引起的RBF减少，表明腺苷对TGF的作用。2）NO：肾内注射加压素（AVP）可引起肾血管收缩。然而，预处理后的V1-拮抗剂，AVP引起显着的血管舒张。用V2受体拮抗剂治疗后，这种血管舒张消失。即使在不存在V2拮抗剂的情况下，肾内输注L-NNA也能减弱血管舒张，L-NNA是NO的抑制剂体外实验：从兔肾显微解剖传入小动脉。synthetase.II.in去甲肾上腺素（NE）以剂量依赖性方式降低了传入小动脉的管腔直径，但血管紧张素II（All）即使在高剂量下也不影响管腔直径。而用L-NNA处理后，所有动物的传入小动脉均收缩。AVP使NE收缩的传入小动脉管腔直径减小，V1受体拮抗剂可抑制AVP的缩血管作用，而V1受体拮抗剂则使NE收缩的传入小动脉管腔直径增大。AVP的这种血管舒张作用可被V2受体拮抗剂阻断。这些发现表明，腺苷发挥了显着的作用，TGF和NO调节各种血管活性物质的行动。少

Renal blood flow remains constant despite wide variations in the perfusion pressure, a phenomenon known as autoregulation. It is now well established that renal autoregulation is mediated by tubuloglomerular feedback (TGF). TGF is a negative feedback system that stabilizes nephronal blood flow, single nephron glomerular filtration rate, and the tubular flow rate. An increase in renal perfusion pressure increases the tubular flow rate via an increase in GFR.The increased tubular flow rate causes an elevation of sodium chloride concentration at the macula densa. This is sensed by the macula densa and results in an increase in the afferent arteriolar resistance. The purpose of the present investigation is determine transmitters that transmit information from the macula densa as a sensor cell to the afferent arteriole as an effector organ. We have focused on an adenosine and nitric oxide (NO) as possible candidates for the transmitter.I.in vivo experiment 1) adenosine : Relationship betwee … More n the renal hemodynamics and the interstitial levels of adenosine was examined in anesthetized dogs. The intrarenal infusion of hypertonic saline resulted in a decrease of renal blood flow (RBF) following a transient increase of RBF and a significant increase of interstitial adenosine concentration. An adenosine 1 receptor antagonist completely blocked the reduction of RBF induced by the hypertonic saline, indicating a role of adenosine for TGF.2) NO : Intrarenal infusion of vasopressin (AVP) resulted in renal vasoconstriction. However, following pretreatment of a V1-antagonist, AVP caused significant vasodilation. This vasodilation disappeared after treatment with the V2-receptor antagonist. Even in the absence of the V2- antagonist, vasodilation was attenuated by intrarenal infusion of L-NNA which is an inhibitor of NO synthetase.II.in vitro experiment : The afferent arterioles were microdissected from the rabbit kidney. Norepinephrine (NE) decreased the lumen diameter of the afferent arteriole in a dose-dependent manner, but angiotensin II (All) even at a high dose did not affect the lumen diameter. However, after treatment with L-NNA,All constricted the afferent arteriole. AVP decreased the lumen diameter of the afferent arteriole and a V1 antagonist inhibited the vasoconstrictor action of AVP.However, AVP increased the lumen diameter of the NE-constricted afferent arteriole pretreated with a V1 antagonist. This vasodilatory effect of AVP was abolished by a V2 antagonist. These findings suggest that adenosine exerts a significant role of TGF and that NO modulates the actions of various vasoactive substances. Less