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A Calcium Paradox in the Context of Neurotransmission



Author(s)

Leandro B. Bergantin, Aron Jurkiewicz, Antonio G. García and Afonso Caricati-Neto

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DOI:10.17265/2328-2150/2015.06.001

The hypothesis of the calcium paradox has its origin in experiments done in neurogenically stimulated rat and mouse vas deferentia. Some old studies reported that reduction of Ca²⁺ entry by mild concentrations of verapamil, diltiazem or nifedipine elicited the surprising augmentation of vas deferens contractions. Recent reports have also found that nifedipine caused a paradoxical augmentation of the exocytotic release of catecholamine elicited by paired depolarising pulses in voltage-clamped bovine chromaffin cells. Because these drugs are blocking the L-subtype of VACCs (voltage-activated calcium channels), augmented contraction and exocytosis was an unexpected outcome. Recent experiments in neurogenically-stimulated rat vas deferens have found a more drastic potentiation of contractions with the association of verapamil and cAMP-enhancer compounds. Thus, the interaction between the signalling pathways mediated by Ca²⁺ and cAMP could explain those unexpected findings and the so-called calcium paradox.

Calcium paradox, cAMP, smooth muscle, sympathetic neurotransmission, chromaffin cell.

Leandro B. Bergantin., et al. 2015. “A Calcium Paradox in the Context of Neurotransmission.” Journal of Pharmacy and Pharmacology 3 (6): 253-261.