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Receptor‐Linked Hydrolysis of Phosphoinositides and Production of Prostacyclin in Cerebral Endothelial Cells
Author(s) -
Xu Jian,
Qu ZhiXiang,
Moore Steven A.,
Hsu Chung Y.,
Hogan Edward L.
Publication year - 1992
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1992.tb10071.x
Subject(s) - prostacyclin , chemistry , hydrolysis , receptor , neuroscience , microbiology and biotechnology , biochemistry , biology
The receptor agonist‐mediated hydrolysis of phosphoinositides and production of prostacyclin were studied in murine cerebral endothelial cells (MCEC). Of 11 neurotransmitters and neuromodulators examined, carbachol, noradrenaline (NE), bradykinin, and thrombin significantly increased 3 H‐inositol phosphate accumulation in the presence of LiCl (20 m M ). The maximal stimulation of [ 3 H]inositol monophosphate ([ 3 H]IP 1 ) reached approximately 11, 11, seven, and four times the basal levels for carbachol, NE, bradykinin, and thrombin, respectively. The EC 50 values of IP 1 accumulation for carbachol and NE were 34 and 0.16 μ M , respectively. The muscarinic antagonists, atropine and pirenzepine, blocked the carbachol‐induced IP 1 accumulation with K i values of 0.3 and 30 n M , respectively. The adrenergic antagonist, prazosin, blocked NE‐induced IP 1 accumulation with a K i of 0.1 n M . The calcium ionophore A23187, histamine, glutamate, vasopressin, serotonin, platelet activating factor, and substance P did not stimulate IP 1 accumulation. A23187, bradykinin, and thrombin stimulated prostacyclin release to approximately four, four, and two times the basal levels, respectively, whereas carbachol and NE had little effect upon prostacyclin release. These results suggest that the activation of phospholipase C and of phospholipase A 2 in MCEC are regulated separately.