Endothelium-derived relaxing factor in pulmonary and renal circulations during hypoxia

M. A. Perrella, Eric Edell, Michael Joseph Krowka, D. A. Cortese, John C Jr. Burnett

Research output: Contribution to journalArticle

55 Citations (Scopus)

Abstract

The pulmonary and renal vasculatures, in contrast to the systemic vasculature, constrict during hypoxia. The endothelium has been implicated in mediating these vascular responses to acute hypoxia via the production of endothelium-derived vasoactive factors. The present study, performed in anesthetized dogs, was designed to investigate the role of endothelium- derived relaxing factor (EDRF) to attenuate the vasoconstrictor response of the pulmonary and renal circulations during acute hypoxia. In response to hypoxia, pulmonary (2.2 ± 0.3 to 4.5 ± 0.6 mmHg · l-1 · min) and renal (0.60 ± 0.07 to 0.90 ± 0.14 mmHg · ml-1 · min) vascular resistances increased. Inhibition of endogenous EDRF with N(G)-monomethyl-L-arginine resulted in similar increases in pulmonary (3.0 ± 0.1 to 4.8 ± 0.4 mmHg · l-1 · min) and renal (0.67 ± 0.07 to 0.90 ± 0.09 mmHg · ml-1 · min) vascular resistances as in hypoxia. However, in the presence of both hypoxia and EDRF inhibition, an exaggerated pulmonary vascular response was observed (2.2 ± 0.2 to 7.4 ± 0.9 mmHg · l-1 · min), in contrast to the renal vascular response to EDRF inhibition during hypoxia (0.61 ± 0.05 to 0.95 ± 0.10 mmHg · ml-1 · min), which was not different from hypoxia or EDRF inhibition individually. The endothelium-derived contracting factor endothelin, which modestly increased during hypoxia (11.7 ± 1.9 to 15.6 ± 2.4 pg/ml), may also contribute to this vasoconstrictive response to hypoxia. This study suggests in the intact animal that EDRF serves to oppose the pulmonary vasoconstrictor response to hypoxia and further characterizes the role of endothelium-derived factors in the regulation of vascular function during hypoxia.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume263
Issue number1 32-1
StatePublished - 1992

Fingerprint

Endothelium-Dependent Relaxing Factors
Pulmonary Circulation
Renal Circulation
Endothelium
Blood Vessels
Lung
Kidney
Vasoconstrictor Agents
Vascular Resistance
Hypoxia
Endothelins
Arginine

Keywords

  • differential regional vascular response
  • hypoxia-induced vasoconstriction
  • intact animal

ASJC Scopus subject areas

  • Physiology

Cite this

@article{5f76eb1769e94b57bd1c044cb8fbc55f,
title = "Endothelium-derived relaxing factor in pulmonary and renal circulations during hypoxia",
abstract = "The pulmonary and renal vasculatures, in contrast to the systemic vasculature, constrict during hypoxia. The endothelium has been implicated in mediating these vascular responses to acute hypoxia via the production of endothelium-derived vasoactive factors. The present study, performed in anesthetized dogs, was designed to investigate the role of endothelium- derived relaxing factor (EDRF) to attenuate the vasoconstrictor response of the pulmonary and renal circulations during acute hypoxia. In response to hypoxia, pulmonary (2.2 ± 0.3 to 4.5 ± 0.6 mmHg · l-1 · min) and renal (0.60 ± 0.07 to 0.90 ± 0.14 mmHg · ml-1 · min) vascular resistances increased. Inhibition of endogenous EDRF with N(G)-monomethyl-L-arginine resulted in similar increases in pulmonary (3.0 ± 0.1 to 4.8 ± 0.4 mmHg · l-1 · min) and renal (0.67 ± 0.07 to 0.90 ± 0.09 mmHg · ml-1 · min) vascular resistances as in hypoxia. However, in the presence of both hypoxia and EDRF inhibition, an exaggerated pulmonary vascular response was observed (2.2 ± 0.2 to 7.4 ± 0.9 mmHg · l-1 · min), in contrast to the renal vascular response to EDRF inhibition during hypoxia (0.61 ± 0.05 to 0.95 ± 0.10 mmHg · ml-1 · min), which was not different from hypoxia or EDRF inhibition individually. The endothelium-derived contracting factor endothelin, which modestly increased during hypoxia (11.7 ± 1.9 to 15.6 ± 2.4 pg/ml), may also contribute to this vasoconstrictive response to hypoxia. This study suggests in the intact animal that EDRF serves to oppose the pulmonary vasoconstrictor response to hypoxia and further characterizes the role of endothelium-derived factors in the regulation of vascular function during hypoxia.",
keywords = "differential regional vascular response, hypoxia-induced vasoconstriction, intact animal",
author = "Perrella, {M. A.} and Eric Edell and Krowka, {Michael Joseph} and Cortese, {D. A.} and Burnett, {John C Jr.}",
year = "1992",
language = "English (US)",
volume = "263",
journal = "American Journal of Physiology - Renal Fluid and Electrolyte Physiology",
issn = "1931-857X",
publisher = "American Physiological Society",
number = "1 32-1",

}

TY - JOUR

T1 - Endothelium-derived relaxing factor in pulmonary and renal circulations during hypoxia

AU - Perrella, M. A.

AU - Edell, Eric

AU - Krowka, Michael Joseph

AU - Cortese, D. A.

AU - Burnett, John C Jr.

PY - 1992

Y1 - 1992

N2 - The pulmonary and renal vasculatures, in contrast to the systemic vasculature, constrict during hypoxia. The endothelium has been implicated in mediating these vascular responses to acute hypoxia via the production of endothelium-derived vasoactive factors. The present study, performed in anesthetized dogs, was designed to investigate the role of endothelium- derived relaxing factor (EDRF) to attenuate the vasoconstrictor response of the pulmonary and renal circulations during acute hypoxia. In response to hypoxia, pulmonary (2.2 ± 0.3 to 4.5 ± 0.6 mmHg · l-1 · min) and renal (0.60 ± 0.07 to 0.90 ± 0.14 mmHg · ml-1 · min) vascular resistances increased. Inhibition of endogenous EDRF with N(G)-monomethyl-L-arginine resulted in similar increases in pulmonary (3.0 ± 0.1 to 4.8 ± 0.4 mmHg · l-1 · min) and renal (0.67 ± 0.07 to 0.90 ± 0.09 mmHg · ml-1 · min) vascular resistances as in hypoxia. However, in the presence of both hypoxia and EDRF inhibition, an exaggerated pulmonary vascular response was observed (2.2 ± 0.2 to 7.4 ± 0.9 mmHg · l-1 · min), in contrast to the renal vascular response to EDRF inhibition during hypoxia (0.61 ± 0.05 to 0.95 ± 0.10 mmHg · ml-1 · min), which was not different from hypoxia or EDRF inhibition individually. The endothelium-derived contracting factor endothelin, which modestly increased during hypoxia (11.7 ± 1.9 to 15.6 ± 2.4 pg/ml), may also contribute to this vasoconstrictive response to hypoxia. This study suggests in the intact animal that EDRF serves to oppose the pulmonary vasoconstrictor response to hypoxia and further characterizes the role of endothelium-derived factors in the regulation of vascular function during hypoxia.

AB - The pulmonary and renal vasculatures, in contrast to the systemic vasculature, constrict during hypoxia. The endothelium has been implicated in mediating these vascular responses to acute hypoxia via the production of endothelium-derived vasoactive factors. The present study, performed in anesthetized dogs, was designed to investigate the role of endothelium- derived relaxing factor (EDRF) to attenuate the vasoconstrictor response of the pulmonary and renal circulations during acute hypoxia. In response to hypoxia, pulmonary (2.2 ± 0.3 to 4.5 ± 0.6 mmHg · l-1 · min) and renal (0.60 ± 0.07 to 0.90 ± 0.14 mmHg · ml-1 · min) vascular resistances increased. Inhibition of endogenous EDRF with N(G)-monomethyl-L-arginine resulted in similar increases in pulmonary (3.0 ± 0.1 to 4.8 ± 0.4 mmHg · l-1 · min) and renal (0.67 ± 0.07 to 0.90 ± 0.09 mmHg · ml-1 · min) vascular resistances as in hypoxia. However, in the presence of both hypoxia and EDRF inhibition, an exaggerated pulmonary vascular response was observed (2.2 ± 0.2 to 7.4 ± 0.9 mmHg · l-1 · min), in contrast to the renal vascular response to EDRF inhibition during hypoxia (0.61 ± 0.05 to 0.95 ± 0.10 mmHg · ml-1 · min), which was not different from hypoxia or EDRF inhibition individually. The endothelium-derived contracting factor endothelin, which modestly increased during hypoxia (11.7 ± 1.9 to 15.6 ± 2.4 pg/ml), may also contribute to this vasoconstrictive response to hypoxia. This study suggests in the intact animal that EDRF serves to oppose the pulmonary vasoconstrictor response to hypoxia and further characterizes the role of endothelium-derived factors in the regulation of vascular function during hypoxia.

KW - differential regional vascular response

KW - hypoxia-induced vasoconstriction

KW - intact animal

UR - http://www.scopus.com/inward/record.url?scp=0026740607&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026740607&partnerID=8YFLogxK

M3 - Article

C2 - 1636793

AN - SCOPUS:0026740607

VL - 263

JO - American Journal of Physiology - Renal Fluid and Electrolyte Physiology

JF - American Journal of Physiology - Renal Fluid and Electrolyte Physiology

SN - 1931-857X

IS - 1 32-1

ER -