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Volume 7, Issue 4 (Suppl) J Neurol Neurophysiol
ISSN:2155-9562 JNN, an open access journal
Page 49
Notes:
Neurology Congress 2016
September 21-23, 2016
conferenceseries.com
September 21-23, 2016 Amsterdam, Netherlands
8th European Neurology Congress
From discovering calcium paradox to Ca2+/cAMP interaction: Impact in human health and disease
Leandro Bueno Bergantin and Afonso Caricati-Neto
UNIFESP-Escola Paulista de Medicina (EPM), Brazil
The 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 neuroprotection in
the neurodegenerative diseases such as Alzheimer´s and Parkinson´s diseases.
Biography
Leandro Bueno Bergantin has received his academic education from UNIFESP-EPM (Brazil) and did his MSc (2010) and PhD (2014) degrees in Biomedicine. His
research involves cell signaling mediated by Ca2+ and cAMP, skeletal and smooth muscles, peripheral and central nervous systems. His research work solved the
enigma of the paradoxical effects produced by L-type Ca2+ channel blockers. He is currently a Post-doctoral fellow (FAPESP) at UNIFESP-EPM.
Leandro Bueno Bergantin et al., J Neurol Neurophysiol 2016, 7:4 (Suppl)