Vascular Myocyte-Derived Nitric Oxide Is an Autocrine That Limits Vasoconstriction

John R. Charpie, R Clinton Webb

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

Vascular myocytes and endothelial cells possess the enzymatic machinery to generate nitric oxide from L-arginine. This study tests the hypothesis that myocyte-derived nitric oxide has an autocrine function to inhibit contraction. Rat aortic rings were placed in muscle baths for isometric force measurement. Denuded and intact rings contracted to Nωnitro-L-arginine; L-arginine reversed these contractions. Compared to intact rings, contractile sensitivity to phenylephrine was increased in denuded rings; Nωnitro-L-arginine caused a further enhancement of phenylephrine sensitivity. Acetylcholine contracted denuded rings but not intact rings; these contractions were also potentiated by Nωnitro-L-arginine. In intact rings contracted with phenylephrine, acetylcholine caused relaxation that was inhibited by Nωnitro-L-arginine. Denuded rings did not relax to acetylcholine. In summary, contractile responses of rat aortae to interventions that alter nitric oxide production are the composite of enzymatic activity in both the endothelial cells and myocytes. Thus, myocyte-derived nitric oxide modulates vascular tone.

Original languageEnglish (US)
Pages (from-to)763-768
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume194
Issue number2
DOIs
StatePublished - Jul 30 1993
Externally publishedYes

Fingerprint

Vasoconstriction
Muscle Cells
Blood Vessels
Arginine
Nitric Oxide
Phenylephrine
Acetylcholine
Endothelial cells
Rats
Endothelial Cells
Force measurement
Baths
Machinery
Muscle
Aorta
Muscles
Composite materials

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

Vascular Myocyte-Derived Nitric Oxide Is an Autocrine That Limits Vasoconstriction. / Charpie, John R.; Webb, R Clinton.

In: Biochemical and Biophysical Research Communications, Vol. 194, No. 2, 30.07.1993, p. 763-768.

Research output: Contribution to journalArticle

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