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  • Short Communication   
  • Cardiovasc Ther 2017, Vol 2(1): 117

The “Calcium Paradox” due to Ca2+/cAMP Interaction and Antihypertensive Pharmacotherapy: New Avenues for Drug Development

Leandro Bueno B* and Caricati Neto A
Department of Pharmacology, Federal University of São Paulo, Escola Paulista de Medicina, Brazil
*Corresponding Author : Leandro Bueno B, Department of Pharmacology, Federal University of São Paulo, Escola Paulista De Medicina, Brazil, Tel: 55-1155764973, Email: leanbio39@yahoo.com.br

Received Date: Mar 09, 2017 / Accepted Date: Mar 21, 2017 / Published Date: Mar 28, 2017

Abstract

In 2013, we showed that the paradoxical effects (sympathetic hyperactivity) induced by L-type voltage-activated Ca2+ channels (VACC) blockers, named by us “calcium paradox” phenomenon, were potentiated by drugs which increase cytosolic cAMP concentration ([cAMP]c-enhancers), for example rolipram, IBMX and forskolin, indicating that the sympathetic hyperactivity induced by VACC blockers is due to interaction of the Ca2+/cAMP intracellular signaling pathways (Ca2+/cAMP interaction). Then, the pharmacological handling of this interaction produced by combined use of the L-type VACC blockers prescribed in the antihypertensive therapy, and [cAMP]c-accumulating compounds prescribed in the antidepressive therapy, could represent a potential cardiovascular deleterious effect for hypertensive patients due to stimulation of sympathetic hyperactivity. Then, we discussed the role of Ca2+/cAMP interaction for antihypertensive pharmacotherapy. In conclusion, this interaction could be a novel therapeutic target for drug development.

Keywords: Ca2+/cAMP interaction; Sympathetic neurotransmission; Hypertension

Citation: Bueno LB, Neto CA (2017) The “Calcium Paradox” due to Ca2+/cAMP Interaction and Antihypertensive Pharmacotherapy: New Avenues for Drug Development. Cardiovasc Ther 2: 117.

Copyright: © 2017 Bueno LB, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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