The dihydropyridine antagonist (-)-202-791 increases calcium channel current amplitude without disrupting the interaction between the channels and activated G proteins in rat sensory neurones.
Does not inform clinical use of calcium channel antagonists; leaves open relevance of G-protein interactions in intact cardiovascular models.
The ability of a depolarizing prepulse to increase the rate of activation of IBa has been examined in cultured sensory neurones of the rat. Both in control neurones and in the presence internally of the guanine nucleotide analogue, guanosine 5'-O-3-thiotriphosphate (GTP gamma S) which markedly slows the rate of activation of IBa and reduces its amplitude, a depolarizing prepulse increased the rate of activation of IBa, but did not increase its amplitude measured at the end of the 100 ms voltage step. The calcium channel antagonist (-)-202-791, which we have previously shown to increase the amplitude of IBa in the presence of GTP gamma S, did not occlude the response to a depolarizing prepulse, suggesting that the mechanism of action of (-)-202-791 is not to disrupt the interaction of the channels with activated G proteins.
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Scott et al. (1990) studied this question.
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