Arendshorst W J, Finn W F
Am J Physiol. 1977 Oct;233(4):F290-7. doi: 10.1152/ajprenal.1977.233.4.F290.
Renal blood flow (RBF) was measured with a noncannulating electromagnetic flow transducer in anesthetized rats which had been maintained for 3-5 wk on low, normal, or high salt plus deoxycorticosterone diets. After base-line observations, one of two dissimilar inhibitors of the renin-angiotensin system, angiotensin I converting enzyme inhibitor SQ 20881 or the structural analogue [Sar1,Ala8]angiotensin II was administered intravenously. The employed doses of SQ 20881 and [Sar1,Ala8]angiotensin II effectively inhibited the pressor and renal vasoconstrictor responses induced by exogenous angiotensin I and II, respectively, in each dietary group. Both inhibitors vasodilated kidneys in salt-restricted rats; however, neither affected base-line renal hemodynamics in salt-loaded rats. Pressure-flow relationships were evaluated by clamping the aorta to reduce renal perfusion pressure. Renal blood flow was autoregulated between 100 and 140 mmHg with the same efficiency before and during inhibition of angiotensin II in each dietary group. These data indicate that angiotensin II modifies base-line RBF and renal vascular resistance and are consistent with the view that the renin-angiotensin system is not an essential mechanism responsible for autoregulation of RBF in the rat.
用非插管式电磁血流传感器在麻醉大鼠中测量肾血流量(RBF),这些大鼠已分别以低、正常或高盐加脱氧皮质酮饮食维持3 - 5周。在基线观察后,静脉注射两种不同的肾素 - 血管紧张素系统抑制剂之一,即血管紧张素I转换酶抑制剂SQ 20881或结构类似物[Sar1,Ala8]血管紧张素II。在每个饮食组中,所使用的SQ 20881和[Sar1,Ala8]血管紧张素II剂量分别有效抑制了外源性血管紧张素I和II诱导的升压和肾血管收缩反应。两种抑制剂均使限盐大鼠的肾脏血管舒张;然而,两者均未影响高盐负荷大鼠的基线肾血流动力学。通过夹闭主动脉以降低肾灌注压来评估压力 - 血流关系。在每个饮食组中,在抑制血管紧张素II之前和期间,肾血流量在100至140 mmHg之间以相同效率进行自身调节。这些数据表明血管紧张素II改变基线RBF和肾血管阻力,并且与肾素 - 血管紧张素系统不是大鼠RBF自身调节的必要机制这一观点一致。