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CNS 2016

December 05-07, 2016

Volume 7, Issue 5(Suppl)

J Neurol Neurophysiol

ISSN: 2155-9562 JNN, an open access journal

conferenceseries

.com

December 05-07, 2016 Dubai, UAE

2

nd

International Conference on

Central Nervous System Disorders & Therapeutics

J Neurol Neurophysiol 2016, 7:5(Suppl)

http://dx.doi.org/10.4172/2155-9562.C1.041

From discovering calcium paradox to Ca

2+

/cAMP interaction: Impact in human health and disease

Leandro Bueno Bergantin and Afonso Caricati-Neto

UNIFESP-Escola Paulista de Medicina (EPM), Brazil

T

he hypothesis of the so-called calcium paradox phenomenon in the sympathetic neurotransmission has its origin in

experiments done in models of neurotransmission since 1970’s. Historically, calcium paradox originated several clinical

studies reporting that acute and chronic administration of L-type Ca2+ Channel Blockers (CCBs), drugs largely used for

antihypertensive therapy such as verapamil and nifedipine produces reduction in peripheral vascular resistance and arterial

pressure, associated with a paradoxical sympathetic hyperactivity. Despite this sympathetic hyperactivity has been initially

attributed to adjust reflex of arterial pressure, the cellular and molecular mechanisms involved in this paradoxical effect of

the L-type CCBs remained unclear for four decades. Also, experimental studies using isolated tissues richly innervated by

sympathetic nerves showed that neurogenic responses were completely inhibited by L-type CCBs in high concentrations, but

paradoxically potentiated in low concentrations, characterized as a calcium paradox phenomenon. We discovered in 2013

that this paradoxical increase in sympathetic activity produced by L-type CCBs is due to Ca2+/cAMP interaction. Then, the

pharmacological manipulation of this interaction could represent a potential cardiovascular risk for hypertensive patients

due to increase of sympathetic hyperactivity. In contrast, this pharmacological manipulation could be a new therapeutic

strategy for increasing neurotransmission in psychiatric disorders such as depression and producing neuro protection in the

neurodegenerative diseases such as Alzheimer´s and Parkinson´s diseases.

leanbio39@yahoo.com.br