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Journal of Neuroscience, Vol 15, 3104-3109, Copyright © 1995 by Society for Neuroscience
cGMP inhibits L-type Ca2+ channel currents through protein phosphorylation in rat pinealocytes
CL Chik, QY Liu, B Li, E Karpinski and AK Ho
Department of Medicine, University of Alberta, Edmonton, Canada.
In this study, the effect of cGMP on the dihydropyridine-sensitive (L-
type) Ca2+ current was investigated using the whole cell version of the
patch-clamp technique in rat pinealocytes. Dibutyryl-cGMP (1 x 10(-4) M)
induced a pronounced inhibition of the L-type Ca2+ channel current. The
dibutyryl-cGMP effect was concentration dependent. Elevation of cGMP by
nitroprusside had a similar inhibitory action on the L-type Ca2+ channel
current. Norepinephrine, which increased cGMP in rat pinealocytes, also
inhibited this current. The action of cGMP was independent of cAMP
elevation since the cAMP antagonist, Rp-cAMPs, had no effect on the
inhibitory action of dibutyryl-cGMP. The involvement of cyclic
GMP-dependent protein kinase was suggested by the blocking action of two
protein kinase inhibitors, (1-(5-isoquinolinesulfonyl)-2- methylpiperazine
(H7) and N-(2-guanidinoethyl)-5- isoquinolinesulfonamide (HA1004), on the
dibutyryl-cGMP effect on the L- type Ca2+ channel current. Taken together,
these results suggest that (1) cGMP modulates L-type Ca2+ channel currents
in rat pinealocytes, causing inhibition of this current; (2) the action of
cGMP appears to be independent of cAMP elevation; and (3) phosphorylation
by cGMP- dependent protein kinase may be involved.
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