Autoregulation of renal blood flow. Effects of indomethacin and ureteral pressure

J. L. Blackshear, Brooks Sayre Edwards, F. G. Knox

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

We tested the hypothesis that there is a common prostaglandin mediated stimulus to arteriolar vasodilation in response to elevated ureteral pressure and reduced arterial perfusion pressure. The responses of renal blood flow (RBF) to reduced renal artery pressure (RAP), elevated ureteral pressure (UP), and reduced RAP superimposed on UP were studied in untreated and indomethacin (I)-treated anesthetized dogs. In untreated dogs, the RBF response was variable, with increases, decreases, or no changes in RBF during reductions in RAP. In contrast, RBF was not increased in any of the I-treated dogs during reduction in RAP, but otherwise the responses were similar to untreated dogs. In the same dogs, RBF responses to elevated UP were evaluated at ureteral pressures of 20, 40, 60, and 80 mm Hg. In untreated dogs, RBF was significantly increased at all levels of elevated UP, while in I-treated dogs RBF did not change at 20, 40, and 60 mm Hg and decreased significantly at 80 mm Hg UP. The response of RBF to reduced RAP was studied in the presence of elevated UP. At 60 mm Hg ureteral pressure, autoregulation of RBF to reduced RAP was abolished in untreated dogs but did not change appreciably in I-treated dogs. We conclude that the renal vasodilation in response to elevated ureteral pressure is mediated by prostaglandins, while the response to reduced perfusion pressure is, for the most part, not mediated by prostaglandins.

Original languageEnglish (US)
Pages (from-to)130-136
Number of pages7
JournalMineral and Electrolyte Metabolism
Volume2
Issue number3
StatePublished - 1979

Fingerprint

Renal Circulation
Indomethacin
Homeostasis
Blood
Pressure
Dogs
Renal Artery
Prostaglandins
Vasodilation
Perfusion

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology, Diabetes and Metabolism

Cite this

Autoregulation of renal blood flow. Effects of indomethacin and ureteral pressure. / Blackshear, J. L.; Edwards, Brooks Sayre; Knox, F. G.

In: Mineral and Electrolyte Metabolism, Vol. 2, No. 3, 1979, p. 130-136.

Research output: Contribution to journalArticle

@article{949db3caeb774416a6f808847daf4dbf,
title = "Autoregulation of renal blood flow. Effects of indomethacin and ureteral pressure",
abstract = "We tested the hypothesis that there is a common prostaglandin mediated stimulus to arteriolar vasodilation in response to elevated ureteral pressure and reduced arterial perfusion pressure. The responses of renal blood flow (RBF) to reduced renal artery pressure (RAP), elevated ureteral pressure (UP), and reduced RAP superimposed on UP were studied in untreated and indomethacin (I)-treated anesthetized dogs. In untreated dogs, the RBF response was variable, with increases, decreases, or no changes in RBF during reductions in RAP. In contrast, RBF was not increased in any of the I-treated dogs during reduction in RAP, but otherwise the responses were similar to untreated dogs. In the same dogs, RBF responses to elevated UP were evaluated at ureteral pressures of 20, 40, 60, and 80 mm Hg. In untreated dogs, RBF was significantly increased at all levels of elevated UP, while in I-treated dogs RBF did not change at 20, 40, and 60 mm Hg and decreased significantly at 80 mm Hg UP. The response of RBF to reduced RAP was studied in the presence of elevated UP. At 60 mm Hg ureteral pressure, autoregulation of RBF to reduced RAP was abolished in untreated dogs but did not change appreciably in I-treated dogs. We conclude that the renal vasodilation in response to elevated ureteral pressure is mediated by prostaglandins, while the response to reduced perfusion pressure is, for the most part, not mediated by prostaglandins.",
author = "Blackshear, {J. L.} and Edwards, {Brooks Sayre} and Knox, {F. G.}",
year = "1979",
language = "English (US)",
volume = "2",
pages = "130--136",
journal = "Mineral and Electrolyte Metabolism",
issn = "0378-0392",
publisher = "S. Karger AG",
number = "3",

}

TY - JOUR

T1 - Autoregulation of renal blood flow. Effects of indomethacin and ureteral pressure

AU - Blackshear, J. L.

AU - Edwards, Brooks Sayre

AU - Knox, F. G.

PY - 1979

Y1 - 1979

N2 - We tested the hypothesis that there is a common prostaglandin mediated stimulus to arteriolar vasodilation in response to elevated ureteral pressure and reduced arterial perfusion pressure. The responses of renal blood flow (RBF) to reduced renal artery pressure (RAP), elevated ureteral pressure (UP), and reduced RAP superimposed on UP were studied in untreated and indomethacin (I)-treated anesthetized dogs. In untreated dogs, the RBF response was variable, with increases, decreases, or no changes in RBF during reductions in RAP. In contrast, RBF was not increased in any of the I-treated dogs during reduction in RAP, but otherwise the responses were similar to untreated dogs. In the same dogs, RBF responses to elevated UP were evaluated at ureteral pressures of 20, 40, 60, and 80 mm Hg. In untreated dogs, RBF was significantly increased at all levels of elevated UP, while in I-treated dogs RBF did not change at 20, 40, and 60 mm Hg and decreased significantly at 80 mm Hg UP. The response of RBF to reduced RAP was studied in the presence of elevated UP. At 60 mm Hg ureteral pressure, autoregulation of RBF to reduced RAP was abolished in untreated dogs but did not change appreciably in I-treated dogs. We conclude that the renal vasodilation in response to elevated ureteral pressure is mediated by prostaglandins, while the response to reduced perfusion pressure is, for the most part, not mediated by prostaglandins.

AB - We tested the hypothesis that there is a common prostaglandin mediated stimulus to arteriolar vasodilation in response to elevated ureteral pressure and reduced arterial perfusion pressure. The responses of renal blood flow (RBF) to reduced renal artery pressure (RAP), elevated ureteral pressure (UP), and reduced RAP superimposed on UP were studied in untreated and indomethacin (I)-treated anesthetized dogs. In untreated dogs, the RBF response was variable, with increases, decreases, or no changes in RBF during reductions in RAP. In contrast, RBF was not increased in any of the I-treated dogs during reduction in RAP, but otherwise the responses were similar to untreated dogs. In the same dogs, RBF responses to elevated UP were evaluated at ureteral pressures of 20, 40, 60, and 80 mm Hg. In untreated dogs, RBF was significantly increased at all levels of elevated UP, while in I-treated dogs RBF did not change at 20, 40, and 60 mm Hg and decreased significantly at 80 mm Hg UP. The response of RBF to reduced RAP was studied in the presence of elevated UP. At 60 mm Hg ureteral pressure, autoregulation of RBF to reduced RAP was abolished in untreated dogs but did not change appreciably in I-treated dogs. We conclude that the renal vasodilation in response to elevated ureteral pressure is mediated by prostaglandins, while the response to reduced perfusion pressure is, for the most part, not mediated by prostaglandins.

UR - http://www.scopus.com/inward/record.url?scp=0018766054&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0018766054&partnerID=8YFLogxK

M3 - Article

AN - SCOPUS:0018766054

VL - 2

SP - 130

EP - 136

JO - Mineral and Electrolyte Metabolism

JF - Mineral and Electrolyte Metabolism

SN - 0378-0392

IS - 3

ER -