Nitric oxide in the control of renal hemodynamics and excretory function

Experimental evidence has now been amassed to indicate that inhibition of nitric oxide (NO) synthase reduces total or regional renal blood flow by approximately 25 to 30% and markedly increases the renal vascular resistance, demonstrating that basal release of NO helps to maintain the relatively low...

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Bibliographic Details
Published in:American journal of hypertension 2001-06, Vol.14 (6), p.74S-82S
Main Authors: Majid, Dewan S.A, Navar, L.Gabriel
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Diuresis - physiology
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Fundamental and applied biological sciences. Psychology
Glomerular Filtration Rate - physiology
Hemodynamics - physiology
Homeostasis - physiology
Kidney - metabolism
Natriuresis - physiology
Nitric Oxide - physiology
pressure natriuresis
Renal autoregulation
Renal Circulation - physiology
renal regional blood flow
Vascular Resistance - physiology
Vertebrates: urinary system
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Summary:Experimental evidence has now been amassed to indicate that inhibition of nitric oxide (NO) synthase reduces total or regional renal blood flow by approximately 25 to 30% and markedly increases the renal vascular resistance, demonstrating that basal release of NO helps to maintain the relatively low vascular resistance that is characteristic for the kidney. It has been demonstrated that intraarterial administration of NO synthase inhibitors causes marked reductions in sodium excretion without changes in filtered load and suppressed the arterial pressure-induced natriuretic responses in the kidney. We also demonstrated that a constant rate infusion of a NO donor in dogs pretreated with a NOS inhibitor resulted in increases in sodium excretion but failed to restore the slope of the relation between arterial pressure and sodium excretion, suggesting that an alteration in intrarenal NO production rate during changes in arterial pressure is involved in the mediation of pressure natriuresis. Further experiments in dogs performed in our laboratory have confirmed that there is a direct relationship between changes in arterial pressure and intrarenal NO activity measured using NO-sensitive microelectrodes in the renal tissue. These arterial pressure-induced changes in intrarenal NO activity were seen positively correlated with the changes in urinary excretion rates of sodium. Collectively, these data suggest that acute changes in arterial pressure alter intrarenal NO production, which inhibits tubular sodium reabsorption to manifest the phenomenon of pressure natriuresis.
ISSN:0895-7061
1879-1905
1941-7225
DOI:10.1016/S0895-7061(01)02073-8