Role of renal nerves, angiotensin II, and prostaglandins in antinatriuretic response to acute hypercapnic acidosis in the dog

R. J. Anderson, W. L. Henrich, P. A. Gross, M. A. Dillingham

Research output: Contribution to journalArticlepeer-review

9 Scopus citations

Abstract

Although clinical studies suggest that chronic hypercapnic acidosis may be associated with renal sodium retention, little information is available on the effect of acute hypercapnic acidosis on renal sodium excretion. The authors, therefore, increased P(CO2) from 23 to 74 mm Hg in anesthetized dogs and observed a marked antinatriuresis as absolute sodium excretion (235 to 60 μEq/min, P <0.001) and fractional excretion of sodium (4.0 to 1.2%, P <0.02) decreased significantly. This decrease in sodium excretion occurred independent of consistent changes in renal perfusion pressure, P(O2), glomerular filtration rate, renal blood flow, extraction of p-aminohippuric acid, and filtration fraction. The antinatriuretic response to acute hypercapnic acidosis could be attenuated significantly by surgical renal denervation, intrarenal phenoxybenzamine, and by intrarenal infusion of 1-sarcosine,8-glycine angiotensin II. Administration of 10 mg/kg indomethacin enhanced the antinatriuretic response to hypercapnic acidosis in denervated kidneys. These results suggest that renal α-adrenergic nerves and the renin angiotensin system result in an antinatriuretic effect during acute hypercapnic acidosis. Renal prostaglandins or related substances may serve to attenuate this antinatriuretic response.

Original languageEnglish (US)
Pages (from-to)294-300
Number of pages7
JournalCirculation research
Volume50
Issue number2
DOIs
StatePublished - Jan 1 1982

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

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