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  • Title: Inhibition by ethaverine of catecholamine secretion through blocking L-type Ca2+ channels in PC12 cells.
    Author: Suh BC, Kim KT.
    Journal: Biochem Pharmacol; 1994 Mar 29; 47(7):1262-6. PubMed ID: 8161356.
    Abstract:
    Ethaverine, a derivative of papaverine, is used as a vasodilator and antispasmodic drug. We have investigated the effects of ethaverine on the secretion of [3H]norepinephrine from PC12 cells, of neuroendocrine origin. Treatment with ethaverine reduced catecholamine secretion in a concentration-dependent manner. The maximal inhibitory effect (90%) was achieved with 10 microM ethaverine, and the IC50 for secretion was approximately 2 microM. Ethaverine pretreatment for 1 min prior to stimulation by 70 mM K+ also decreased the level of intracellular Ca2+ in a concentration-dependent manner, as measured by fura-2 fluorescence. The IC50 for the inhibition of the increase in intracellular Ca2+ was approximately 2 microM. Nifedipine, a dihydropyridine L-type Ca2+ channel blocker, did not enhance the inhibitory effect of ethaverine on the 70 mM K(+)-induced increase in [Ca2+]i or catecholamine secretion. In contrast, the addition of the N-type voltage-sensitive Ca2+ channel antagonist omega-conotoxin with ethaverine resulted in further reductions in the increase in [Ca2+]i and catecholamine release. Maximally effective concentrations of ethaverine and nifedipine showed the same inhibitory effect on the 70 mM K(+)-evoked responses. However, ethaverine pretreatment did not inhibit the bradykinin-induced secretion and [Ca2+]i rise, which are known to be produced through the receptor-operated Ca2+ channels. We conclude that ethaverine reduces catecholamine secretion by blocking the L-type voltage-sensitive Ca2+ channel.
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