Affiliation

Department of Pharmacology, Escola Paulista de Medicina, Universidade Federal de São Paulo (UNIFESP); E-mail: leanbio39@yahoo.com.br

Corresponding Author

Leandro Bueno Bergantin, Department of Pharmacology, Escola Paulista de Medicina, Universidade Federal de São Paulo (UNIFESP); E-mail: leanbio39@yahoo.com.br

Citation

Bergantin, L.B., Caricati-Neto, A. New Concepts for Clinical Pathology from Ca²⁺/Camp Signalling Interaction. (2017) J Clin Trials Pathol Case Stud 2(1): 1- 3.

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© 2017 Bergantin, L.B. This is an Open access article distributed under the terms of Creative Commons Attribution 4.0 International License.

Keywords

Abstract

  It is now well-accepted that the interaction between intracellular signalling pathways mediated by Ca²⁺ and cAMP (Ca²⁺/cAMP signalling interaction) plays as a key role in cellular processes of mammalians. In the clinical pathology field, it has opened a new avenue for the drug development more effective, and safer, for the treatment of neurodegenerative diseases. It has been almost 4 years since we revealed the involvement of the Ca²⁺/cAMP signalling interaction in the enigma of the so-called “calcium paradox”. Interestingly, the “calcium paradox” initiated decades ago, when numerous clinical studies have reported that prescription of L-type Ca²⁺ channel blockers (CCBs) for hypertensive patients decreased arterial pressure, but produced typical symptoms of sympathetic hyperactivity. Despite these adverse effects of CCBs have been initially attributed to adjust reflex of arterial pressure, during almost four decades this enigmatic phenomenon (the so-called “calcium paradox”) remained unclear. In 2013, through an ingenious experiment, we discovered that this phenomenon was resulting of increment of transmitter release from sympathetic neurons, and adrenal chromaffin cells, stimulated by CCBs due to its interference on the Ca²⁺/cAMP signalling interaction. Thus, pharmacological handling of the Ca²⁺/cAMP signaling interaction could be a more efficient and safer therapeutic strategy for stimulating neurotransmission compromised by neurotransmitter release deficit, and attenuating neuronal death.