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J Biol Chem, Vol. 273, Issue 8, 4695-4704, February 20, 1998
1 VIA G
q/11 AND
TO PLC-
3 VIA G
i3
From the Departments of Medicine and Physiology, Medical College of
Virginia, Richmond, Virginia 23298-0711
P2 receptor subtypes and their
signaling mechanisms were characterized in dispersed smooth muscle
cells. UTP and ATP stimulated inositol 1,4,5-triphosphate formation,
Ca2+ release, and contraction that were abolished by
U-73122 and guanosine 5'-O-(3-thio)diphosphate, and partly
inhibited (50-60%) by pertussis toxin (PTX). ATP analogs
(adenosine 5'-( ATP and UTP activated Gq/11 and
Gi3 in gastric and aortic smooth muscle and heart
membranes, Gq/11 and Gi1 and/or
Gi2 in liver membranes, and Go and
Gi1-3 in brain membranes. Phosphoinositide hydrolysis stimulated by ATP and UTP was mediated concurrently by
G The pattern of responses implied that P2Y2 receptors in
visceral, and probably vascular, smooth muscle are coupled to PLC-
,
-methylene)triphosphate, adenosine
5'-(
,
-methylene)triphosphate, and 2-methylthio-ATP) stimulated Ca2+ influx and contraction that were abolished
by nifedipine and in Ca2+-free medium. Micromolar
concentrations of ATP stimulated both Ca2+ influx and
Ca2+ release.
q/11-dependent activation of
phospholipase (PL) C-
1 and
G
i3-dependent activation of
PLC-
3. Phosphoinositide hydrolysis was partially inhibited by PTX or
by antibodies to G
q/11, G
,
PLC-
1, or PLC-
3, and completely inhibited by the following
combinations (PLC-
1 and PLC-
3 antibodies;
G
q/11 and G
antibodies; PLC-
1
and G
antibodies; PTX with either PLC-
1 or
G
q/11 antibody).
1 via G
q/11 and to PLC-
3 via
G
i3. These receptors co-exist with
ligand-gated P2X1 receptors activated by ATP analogs and
high levels of ATP.
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