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

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. We, therefore, increased PCO2 from 23 to 74 mm Hg in anesthetized dogs and observed a marked antinatriuresis as absolute sodium excretion (235 to 60 muEq/min, P less than 0.001) and fractional excretion of sodium (4.0 to 1.2 %, P less than 0.02) decreased significantly. This decrease in sodium excretion occurred independent of consistent changes in renal perfusion pressure, PO2, 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 alpha-adrenergic nerves and the renal angiotensin system result in an antinatriuretic effect during acute hypercapnic acidosis. Renal prostaglandins or related substances may serve to attenuate this antinatriuretic response.

journal_name

Circ Res

journal_title

Circulation research

authors

Anderson RJ,Henrich WL,Gross PA,Dillingham MA

doi

10.1161/01.res.50.2.294

subject

Has Abstract

pub_date

1982-02-01 00:00:00

pages

294-300

issue

2

eissn

0009-7330

issn

1524-4571

journal_volume

50

pub_type

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