Document Detail


Nitric oxide in the control of renal hemodynamics and excretory function.
MedLine Citation:
PMID:  11411769     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
D S Majid; L G Navar
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review    
Journal Detail:
Title:  American journal of hypertension     Volume:  14     ISSN:  0895-7061     ISO Abbreviation:  Am. J. Hypertens.     Publication Date:  2001 Jun 
Date Detail:
Created Date:  2001-06-19     Completed Date:  2001-12-04     Revised Date:  2009-02-24    
Medline Journal Info:
Nlm Unique ID:  8803676     Medline TA:  Am J Hypertens     Country:  United States    
Other Details:
Languages:  eng     Pagination:  74S-82S     Citation Subset:  IM    
Affiliation:
Department of Physiology, Tulane University Health Sciences Center, New Orleans, Louisiana 70112, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Diuresis / physiology*
Feedback
Glomerular Filtration Rate / physiology
Hemodynamics / physiology
Homeostasis / physiology
Kidney / metabolism
Natriuresis / physiology
Nitric Oxide / physiology*
Renal Circulation / physiology*
Vascular Resistance / physiology
Grant Support
ID/Acronym/Agency:
HL 18426/HL/NHLBI NIH HHS; HL 51306/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
10102-43-9/Nitric Oxide

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