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J. Biol. Chem., Vol. 262, Issue 15, 6947-6950, 05, 1987
JP Galizzi, J Qar, M Fosset, C Van Renterghem and M Lazdunski
Voltage-dependent Ca2+ channels of the aortic cell line A7r5 were studied
using 45Ca2+ flux experiments. Ca2+ channels which have been studied belong
to the L-type and are very sensitive to inhibitors and activators in the
1,4-dihydropyridine series as well as to (- )desmethoxyverapamil and
d-cis-diltiazem. L-type Ca2+ channels in these smooth muscle cells are not
affected by cyclic 8-bromo-AMP and dibutyryl cyclic AMP. However, the
activity of these channels is strongly depressed after treatment with
diacylglycerols (1-oleyl 2- acetylglycerol and 1,2-dioctanoylglycerol).
Phorbol esters, which like diacylglycerols are well-known activators of
protein kinase C (the Ca2+- and phospholipid-dependent enzyme), inhibit 70%
of Ca2+ channel activity (K0.5 = 25 nM for phorbol 12-myristate 13-acetate
and K0.5 = 200 nM for phorbol 12,13-dibutyrate). Phorbol esters that are
inactive on kinase C are without effect on Ca2+ channel activity.
[Arg8]Vasopressin and bombesin, two peptides that are well known for their
action on polyphosphoinositide metabolism, inhibit Ca2+ channel activity to
the same extent as active phorbol esters (65-70%). Oxytocin has the same
type of effect presumably by acting at the V1-receptor. Both effects of
[Arg8]vasopressin and oxytocin are suppressed by [1-
(beta-mercapto-beta,beta-diethylpropionic acid)4-valine]arginine
vasopressin, a specific vasopressin antagonist at the V1-receptor.
Regulation of calcium channels in aortic muscle cells by protein kinase C activators (diacylglycerol and phorbol esters) and by peptides (vasopressin and bombesin) that stimulate phosphoinositide breakdown
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