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: The role of sarcoplasmic reticulum in endothelium-dependent and endothelium-independent rhythmic contractions in the rabbit mesenteric artery.
    Author: Omote M, Mizusawa H.
    Journal: Acta Physiol Scand; 1993 Sep; 149(1):15-21. PubMed ID: 8237418.
    Abstract:
    Upon stimulation with phenylephrine, the rabbit mesenteric artery displays endothelium-dependent and endothelium-independent rhythmic contractions in the absence and the presence of ryanodine, respectively. For examination of the involvement of the sarcoplasmic reticulum (SR) in these two types of rhythmic contractions, the mesenteric ring was suspended in an organ chamber for isometric tension recordings. Phenylephrine induced endothelium-dependent rhythmic contractions (EDRC), which were converted to endothelium-independent rhythmic contractions (EIRC) by the subsequent addition of ryanodine. Cyclopiazonic acid (CPA) also induced EIRC in the artery contracted with phenylephrine. The nifedipine-treated artery displayed neither EDRC upon phenylephrine stimulation nor EIRC by the addition of ryanodine or CPA: however, these agents relaxed the arteries. Phenylephrine induced EDRC in the artery treated with the K+ channel antagonist sparteine, but these rhythmic contractions were converted to a sustained contraction by ryanodine and CPA without producing relaxation of the artery. Ryanodine and CPA inhibited both phenylephrine-induced Ca2+ release from the SR and Ca2+ sequestration, without affecting Ca2+ influx across the plasmalemma, evaluated by monitoring agonist-induced contractions. These findings indicate that: (1) the EDRC may be attributed to Ca2+ release from the SR, which may be charged by Ca2+ influx via the voltage-dependent Ca2+ channel; and (2) the EIRC may arise from functional impairment of the SR and by the subsequent increase in the K+ efflux, presumably via the Ca(2+)-activated K+ channel.
    [Abstract] [Full Text] [Related] [New Search]