INHIBITION OF NITRIC-OXIDE SYNTHESIS ATTENUATES PRESSURE-INDUCED NATRIURETIC RESPONSES IN ANESTHETIZED DOGS

被引:186
作者
MAJID, DSA
WILLIAMS, A
NAVAR, LG
机构
来源
AMERICAN JOURNAL OF PHYSIOLOGY | 1993年 / 264卷 / 01期
关键词
RENAL HEMODYNAMICS; RENAL AUTOREGULATION; RENAL FUNCTION; NITRO-L-ARGININE; ANGIOTENSIN-II RECEPTOR ANTAGONIST; LOSARTAN;
D O I
10.1152/ajprenal.1993.264.1.F79
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Inhibition of nitric oxide (NO) synthesis by intrarenal administration of nitro-L-arginine (NLA) leads to decreases in urinary sodium excretion (U(Na)V) in association with the increases in renal vascular resistance (RVR). In the present study, we examined the ability of the kidney to alter its sodium excretion in response to acute changes in renal arterial pressure (RAP) in anesthetized dogs before and during intrarenal infusion of NLA (50 mug.kg-I.min-1). NO synthesis inhibition in 11 dogs increased RVR by 32 +/- 4% and decreased renal blood flow (RBF) by 25 +/- 3%, outer cortical blood flow by 25 +/- 6%, urine flow by 37 +/- 14%, U(Na)V by 71 +/- 5%, and fractional excretion of sodiUM (FE(Na)) by 71 +/- 4%. Glomerular filtration rate was not significantly changed during NLA infusion. As previously reported, there was suppression of the RBF autoregulation plateau during NO synthesis inhibition. In addition, there was a marked attenuation of urine flow and U(Na)V responses to reductions in RAP (150 to 75 mmHg), with significant reductions in the slopes of the relationships between RAP vs. U(Na)V and RAP vs. FE(Na) during NLA infusion. Similar responses were observed in nine other dogs treated with the angiotensin receptor antagonist losartan, indicating that an augmented activity of the renin-angiotensin system is not responsible for attenuation of the slope of the pressure-natriuresis relationship during NLA infusion. These data suggest that NO may participate in the mediation of the pressure-natriuresis response.
引用
收藏
页码:F79 / F87
页数:9
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