Role of nitric oxide in renal papillary blood flow and sodium excretion. Hypertension 1992 Jun;19(6 Pt 2):766-9
Date
06/11/1992Pubmed ID
1592478DOI
10.1161/01.hyp.19.6.766Scopus ID
2-s2.0-0026602775 (requires institutional sign-in at Scopus site) 218 CitationsAbstract
Renal medullary interstitial infusion of NG-nitro-L-arginine (120 micrograms/hr, n = 7) decreased papillary blood flow to 71 +/- 5% of control without altering outer cortical flow. Before NG-nitro-L-arginine infusion, interstitial acetylcholine administration (200 micrograms/hr) increased cortical and papillary blood flow to 134 +/- 6% and 113 +/- 2% of control, respectively. After NG-nitro-L-arginine administration, the vasodilator response to acetylcholine was abolished. In clearance experiments, renal medullary infusion of NG-nitro-L-arginine (120 micrograms/hr, n = 7) significantly decreased total renal blood flow by 10%, renal interstitial fluid pressure by 23%, sodium excretion by 34%, and urine flow by 39% without altering glomerular filtration rate, fractional sodium and water excretion, blood pressure, or urine osmolality. These data indicate that selective inhibition of nitric oxide in the renal medullary vasculature reduces papillary blood flow, which is associated with decreased sodium and water excretion. We conclude that nitric oxide exerts a tonic influence on the renal medullary circulation.
Author List
Mattson DL, Roman RJ, Cowley AW JrAuthor
Allen W. Cowley Jr PhD Professor in the Physiology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsArginine
Diuresis
Extracellular Space
Injections
Injections, Intra-Arterial
Kidney
Kidney Medulla
Male
Natriuresis
Nitric Oxide
Nitroarginine
Pressure
Rats
Rats, Inbred Strains
Regional Blood Flow
Renal Circulation