J. Biol. Chem., Vol. 256, Issue 19, 9990-9993, 10, 1981
Inhibitory effects of sodium and other monovalent cations on human platelet adenylate cyclase
ML Steer and A Wood
Both basal and prostaglandin E1 (PGE1)-stimulated human platelet adenylate
cyclase activity are inhibited by Na+ and other monovalent cations.
Inhibition occurs when the cations are present in concentrations of 20 to
120 mM. Inhibition of basal activity by epinephrine requires the presence
of GTP but not Na+. In the presence of epinephrine and GTP, Na+ further
reduces basal activity, and the combined effects of all three ligands
results in a 70% reduction of basal activity. Sodium, however, does not
increase the fractional inhibition of basal activity attributable to
epinephrine. Sodium increases the concentrations of epinephrine and of PGE1
required for half-maximal inhibition and stimulation of adenylate cyclase
but does not alter the apparent km for Mg2+ or ATP. The rate and extent of
adenylate cyclase activation by the GTP analog guanyl-5'-yl
imidodiphosphate is reduced by Na+, although the cation does not prevent
the acceleration of activation by guanyl-5'-yl imidodiphosphate induced by
PGE1. Other monovalent cations also inhibit the platelet cyclase with an
order of potency of Na+ greater than Li+ greater than K+ greater than
choline+. In addition to demonstrating that Na+ is not required for
hormonal inhibition of platelet adenylate cyclase, these studies
demonstrate the multiple inhibitory effects which can be induced by Na+ and
other monovalent cations. The pattern of these effects suggests that the
cations interfere with functional coupling between receptors, guanine
nucleotide binding units, and catalytic units of the adenylate cyclase
complex.
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