Abstract
The sympathetic hyperactivity due to increment of catecholamine plasma levels, and tachycardia, is the main adverse effect reported since 70's by hypertensive patients that use L-type Ca2+ channel blockers (CCBs). Our discovery of the involvement of interaction between the intracellular signalling pathways mediated by Ca2+ and cAMP (Ca2+/cAMP interaction) revealed that the sympathetic hyperactivity was resulting of increase of transmitter release from sympathetic neurons stimulated by CCBs due to its interference on the Ca2+/cAMP interaction. In the pharmacotherapy of Parkinson's disease, this discovery may produce new paths for the understanding of the cellular and molecular mechanisms involved in the pathogenesis of this disease. In this way, novel journeys for the development of new pharmacological strategies more effective for the treatment of Parkinson's may be initiated.
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