These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Vascular myocyte-derived nitric oxide is an autocrine that limits vasoconstriction.
    Author: Charpie JR, Webb RC.
    Journal: Biochem Biophys Res Commun; 1993 Jul 30; 194(2):763-8. PubMed ID: 8343158.
    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 N omega nitro-L-arginine; L-arginine reversed these contractions. Compared to intact rings, contractile sensitivity to phenylephrine was increased in denuded rings; N omega nitro-L-arginine caused a further enhancement of phenylephrine sensitivity. Acetylcholine contracted denuded rings but not intact rings; these contractions were also potentiated by N omega nitro-L-arginine. In intact rings contracted with phenylephrine, acetylcholine caused relaxation that was inhibited by N omega nitro-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.
    [Abstract] [Full Text] [Related] [New Search]