Effects of phospholipase C inhibitors on Ca2+ channel stimulation and Ca2+ release from intracellular stores evoked by α1A- and α2A-adrenoceptors in rat portal vein myocytes

Nathalie Macrez-Leprêtre, Jean-Luc Morel, Jean Mironneau
Biochemical and Biophysical Research Communications. 1996-01-01; 218(1): 30-34
DOI: 10.1006/bbrc.1996.0006

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1. Biochem Biophys Res Commun. 1996 Jan 5;218(1):30-4.

Effects of phospholipase C inhibitors on Ca2+ channel stimulation and Ca2+
release from intracellular stores evoked by alpha 1A- and alpha 2A-adrenoceptors
in rat portal vein myocytes.

Macrez-Leprêtre N(1), Morel JL, Mironneau J.

Author information:
(1)Laboratoire de Physiologie Cellulaire et Pharmacologie Moléculaire, URA CNRS
1489, Université de Bordeaux II, France.

The ability of phospholipase C inhibitors to inhibit Ca2+ channel stimulation and
Ca2+ release from intracellular stores evoked by norepinephrine in single rat
portal vein myocytes was investigated in the aim of identifying the type of
phospholipase C involved in the transduction pathways activated by alpha 1A- and
alpha 2A-adrenoceptors. U73122 (an inhibitor of
phosphatidylinositol-phospholipase C) inhibited in a concentration-dependent
manner the release of Ca2+ from the intracellular stores induced by activation of
alpha 1A-adrenoceptors and related to inositol phosphate production whereas
U73343 was ineffective. Both compounds had no effect on the release of Ca2+
induced by caffeine. However, U73122 and U73343 inhibited the L-type Ca2+
channel. D609 (an inhibitor of phosphatidylcholine-phospholipase C) had no direct
inhibitory effects on the L-type Ca2+ channel but it inhibited concentration
dependently the alpha 2A-adrenoceptor-induced stimulation of Ca2+ channels, which
had been shown to be independent of phosphatidylinositol hydrolysis. Therefore,
these results suggest that alpha 2A-adrenoceptors activate a
phosphatidylcholine-phospholipase C in vascular myocytes. However, D609 had other
sites of action as it blocked norepinephrine- and caffeine-induced Ca2+ release
from the intracellular stores.

DOI: 10.1006/bbrc.1996.0006
PMID: 8573150 [Indexed for MEDLINE]

Auteurs Bordeaux Neurocampus