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

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

Research output: Contribution to journalArticle

9 Citations (Scopus)

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
StatePublished - 1982
Externally publishedYes

Fingerprint

Acidosis
Angiotensin II
Prostaglandins
Dogs
Kidney
Sodium
p-Aminohippuric Acid
Phenoxybenzamine
Renal Circulation
Denervation
Renin-Angiotensin System
Glomerular Filtration Rate
Indomethacin
Adrenergic Agents
Glycine
Perfusion
Pressure

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Role of renal nerves, angiotensin II, and prostaglandins in antinatriuretic response to acute hypercapnic acidosis in the dog. / Anderson, R. J.; Henrich, William L; Gross, P. A.; Dillingham, M. A.

In: Circulation Research, Vol. 50, No. 2, 1982, p. 294-300.

Research output: Contribution to journalArticle

@article{f6780129bca14b1ab556cd205ee7bcfd,
title = "Role of renal nerves, angiotensin II, and prostaglandins in 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. 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.",
author = "Anderson, {R. J.} and Henrich, {William L} and Gross, {P. A.} and Dillingham, {M. A.}",
year = "1982",
language = "English (US)",
volume = "50",
pages = "294--300",
journal = "Circulation Research",
issn = "0009-7330",
publisher = "Lippincott Williams and Wilkins",
number = "2",

}

TY - JOUR

T1 - Role of renal nerves, angiotensin II, and prostaglandins in antinatriuretic response to acute hypercapnic acidosis in the dog

AU - Anderson, R. J.

AU - Henrich, William L

AU - Gross, P. A.

AU - Dillingham, M. A.

PY - 1982

Y1 - 1982

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0020030362&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0020030362&partnerID=8YFLogxK

M3 - Article

C2 - 7055860

AN - SCOPUS:0020030362

VL - 50

SP - 294

EP - 300

JO - Circulation Research

JF - Circulation Research

SN - 0009-7330

IS - 2

ER -