Abstract
Despite the marked differences in their chemical structure, members of a heterogeneous group of pharmacological agents are thought specifically to block Ca2+ influx through calcium channels1 and thus mediate negative inotropic cardiac effects and vasodilatation. Electrophysiological studies of the myocardium have shown that the slow inward Ca2+ current is blocked1, but the cellular mechanism of these agents in vascular smooth muscle is largely unknown. Felodipine [4-(2,3-dichlorophenyl)-1,4-dihydropyridine-2,6-dimethyl 3,5-dicarboxylic 3-ethylester and 5-methylester)] is a new antihypertensive agent which seems specifically to dilate precapillary resistance vessels in vivo. It is a structural analogue of nifedipine1 and SKF 242602, both of which have been classified as ‘calcium antagonists’, implying that their vascular as well as myocardial actions are due to a blockade of Ca2+ influx. However, the findings reported here point rather to an interaction between felodipine and calcium-binding proteins such as calmodulin.
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Boström, SL., Ljung, B., Mårdh, S. et al. Interaction of the antihypertensive drug felodipine with calmodulin. Nature 292, 777–778 (1981). https://doi.org/10.1038/292777a0
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DOI: https://doi.org/10.1038/292777a0
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