Does endothelin-1 mediate endothelium-dependent contractions during anoxia?

P. M. Vanhoutte, W. Auch-Schwelk, C. Boulanger, P. A. Janssen, Zvonimir S Katusic, K. Komori, Virginia M Miller, V. B. Schini, M. Vidal

Research output: Contribution to journalArticle

67 Citations (Scopus)

Abstract

Endothelin-1 (ET-1) is a more potent constrictor of femoral venous than femoral arterial smooth muscle. By contrast, endothelium-dependent contractions to anoxia are more prominent in the artery. Unlike those to ET-1, the endothelium-dependent contractions evoked by anoxia are rapid in onset and readily reversible; they are antagonized by Ca2+ entry blockers. ET-1-induced responses are inhibited by endothelium-dependent relaxing factors in canine arteries, and to a lower extent in veins. ET-1 does not augment the production of cyclic GMP in cultured porcine aortic endothelial cells, or in canine arteries and veins, suggesting that the peptide does not evoke the release of endothelium-dependent relaxing factor (EDRF) in canine blood vessels. The endothelium-derived contracting factor (EDCF) released during anoxic contraction cannot be bioassayed, under conditions where ET-1 causes contraction of the bioassay tissue. No ET-1 appears to be released in the extracellular space during anoxic contractions. These findings do not support the hypothesis that ET-1 is the EDCF released by anoxia.

Original languageEnglish (US)
JournalJournal of Cardiovascular Pharmacology
Volume13
Issue numberSUPPL. 5
StatePublished - 1989

Fingerprint

Endothelin-1
Endothelium
Canidae
Endothelium-Dependent Relaxing Factors
Arteries
Thigh
Veins
Cyclic GMP
Extracellular Space
Hypoxia
Biological Assay
Smooth Muscle
Blood Vessels
Swine
Endothelial Cells
Peptides

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Pharmacology

Cite this

Vanhoutte, P. M., Auch-Schwelk, W., Boulanger, C., Janssen, P. A., Katusic, Z. S., Komori, K., ... Vidal, M. (1989). Does endothelin-1 mediate endothelium-dependent contractions during anoxia? Journal of Cardiovascular Pharmacology, 13(SUPPL. 5).

Does endothelin-1 mediate endothelium-dependent contractions during anoxia? / Vanhoutte, P. M.; Auch-Schwelk, W.; Boulanger, C.; Janssen, P. A.; Katusic, Zvonimir S; Komori, K.; Miller, Virginia M; Schini, V. B.; Vidal, M.

In: Journal of Cardiovascular Pharmacology, Vol. 13, No. SUPPL. 5, 1989.

Research output: Contribution to journalArticle

Vanhoutte, PM, Auch-Schwelk, W, Boulanger, C, Janssen, PA, Katusic, ZS, Komori, K, Miller, VM, Schini, VB & Vidal, M 1989, 'Does endothelin-1 mediate endothelium-dependent contractions during anoxia?', Journal of Cardiovascular Pharmacology, vol. 13, no. SUPPL. 5.
Vanhoutte PM, Auch-Schwelk W, Boulanger C, Janssen PA, Katusic ZS, Komori K et al. Does endothelin-1 mediate endothelium-dependent contractions during anoxia? Journal of Cardiovascular Pharmacology. 1989;13(SUPPL. 5).
Vanhoutte, P. M. ; Auch-Schwelk, W. ; Boulanger, C. ; Janssen, P. A. ; Katusic, Zvonimir S ; Komori, K. ; Miller, Virginia M ; Schini, V. B. ; Vidal, M. / Does endothelin-1 mediate endothelium-dependent contractions during anoxia?. In: Journal of Cardiovascular Pharmacology. 1989 ; Vol. 13, No. SUPPL. 5.
@article{82c38c05626b48c1853909ff9027cc48,
title = "Does endothelin-1 mediate endothelium-dependent contractions during anoxia?",
abstract = "Endothelin-1 (ET-1) is a more potent constrictor of femoral venous than femoral arterial smooth muscle. By contrast, endothelium-dependent contractions to anoxia are more prominent in the artery. Unlike those to ET-1, the endothelium-dependent contractions evoked by anoxia are rapid in onset and readily reversible; they are antagonized by Ca2+ entry blockers. ET-1-induced responses are inhibited by endothelium-dependent relaxing factors in canine arteries, and to a lower extent in veins. ET-1 does not augment the production of cyclic GMP in cultured porcine aortic endothelial cells, or in canine arteries and veins, suggesting that the peptide does not evoke the release of endothelium-dependent relaxing factor (EDRF) in canine blood vessels. The endothelium-derived contracting factor (EDCF) released during anoxic contraction cannot be bioassayed, under conditions where ET-1 causes contraction of the bioassay tissue. No ET-1 appears to be released in the extracellular space during anoxic contractions. These findings do not support the hypothesis that ET-1 is the EDCF released by anoxia.",
author = "Vanhoutte, {P. M.} and W. Auch-Schwelk and C. Boulanger and Janssen, {P. A.} and Katusic, {Zvonimir S} and K. Komori and Miller, {Virginia M} and Schini, {V. B.} and M. Vidal",
year = "1989",
language = "English (US)",
volume = "13",
journal = "Journal of Cardiovascular Pharmacology",
issn = "0160-2446",
publisher = "Lippincott Williams and Wilkins",
number = "SUPPL. 5",

}

TY - JOUR

T1 - Does endothelin-1 mediate endothelium-dependent contractions during anoxia?

AU - Vanhoutte, P. M.

AU - Auch-Schwelk, W.

AU - Boulanger, C.

AU - Janssen, P. A.

AU - Katusic, Zvonimir S

AU - Komori, K.

AU - Miller, Virginia M

AU - Schini, V. B.

AU - Vidal, M.

PY - 1989

Y1 - 1989

N2 - Endothelin-1 (ET-1) is a more potent constrictor of femoral venous than femoral arterial smooth muscle. By contrast, endothelium-dependent contractions to anoxia are more prominent in the artery. Unlike those to ET-1, the endothelium-dependent contractions evoked by anoxia are rapid in onset and readily reversible; they are antagonized by Ca2+ entry blockers. ET-1-induced responses are inhibited by endothelium-dependent relaxing factors in canine arteries, and to a lower extent in veins. ET-1 does not augment the production of cyclic GMP in cultured porcine aortic endothelial cells, or in canine arteries and veins, suggesting that the peptide does not evoke the release of endothelium-dependent relaxing factor (EDRF) in canine blood vessels. The endothelium-derived contracting factor (EDCF) released during anoxic contraction cannot be bioassayed, under conditions where ET-1 causes contraction of the bioassay tissue. No ET-1 appears to be released in the extracellular space during anoxic contractions. These findings do not support the hypothesis that ET-1 is the EDCF released by anoxia.

AB - Endothelin-1 (ET-1) is a more potent constrictor of femoral venous than femoral arterial smooth muscle. By contrast, endothelium-dependent contractions to anoxia are more prominent in the artery. Unlike those to ET-1, the endothelium-dependent contractions evoked by anoxia are rapid in onset and readily reversible; they are antagonized by Ca2+ entry blockers. ET-1-induced responses are inhibited by endothelium-dependent relaxing factors in canine arteries, and to a lower extent in veins. ET-1 does not augment the production of cyclic GMP in cultured porcine aortic endothelial cells, or in canine arteries and veins, suggesting that the peptide does not evoke the release of endothelium-dependent relaxing factor (EDRF) in canine blood vessels. The endothelium-derived contracting factor (EDCF) released during anoxic contraction cannot be bioassayed, under conditions where ET-1 causes contraction of the bioassay tissue. No ET-1 appears to be released in the extracellular space during anoxic contractions. These findings do not support the hypothesis that ET-1 is the EDCF released by anoxia.

UR - http://www.scopus.com/inward/record.url?scp=0024506465&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024506465&partnerID=8YFLogxK

M3 - Article

C2 - 2473285

AN - SCOPUS:0024506465

VL - 13

JO - Journal of Cardiovascular Pharmacology

JF - Journal of Cardiovascular Pharmacology

SN - 0160-2446

IS - SUPPL. 5

ER -