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: Modulation of Ca2+ channels by alpha 1A- and alpha 2A-adrenoceptors in vascular myocytes: involvement of different transduction pathways.
    Author: Mironneau J, Macrez-Leprêtre N.
    Journal: Cell Signal; 1995 Jul; 7(5):471-9. PubMed ID: 8562308.
    Abstract:
    Using subtype-selective agonists and antagonists, and antibodies directed against phosphatidylinositol and G-proteins, it has been shown in single myocytes of rat portal vein that both alpha 1A- and alpha 2A-adrenoceptors modulate Ca2+ channels through two distinct transduction pathways. alpha 1A-adrenoceptors couple with a Gq/G11 protein to activate a phospholipase C (PLC) which hydrolyses phosphatidylinositol to generate inositol 1,4,5-trisphosphate (InsP3) and diacylglycerol (DAG). InsP3 releases intracellular stored Ca2+ as evidenced by microspectrofluorimetry with Fura-2. The large and transient increase in [Ca2+]i activates chloride channels leading to a membrane depolarization that opens voltage-gated Ca2+ channels. In addition, DAG activates transiently protein kinase C (PKC) which increases the opening probability of Ca2+ channels through a phosphorylation-dependent process. alpha 2A-adrenoceptors do not induce Ca2+ release from intracellular stores but promote sustained Ca2+ influx through voltage-gated Ca2+ channels. The coupling involves a Gi-protein and activation of PKC by DAG. These two transduction pathways may be involved in the physiological action of noradrenaline in vascular smooth muscles.
    [Abstract] [Full Text] [Related] [New Search]