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T-type calcium channels in rat carotid body chemoreceptor cells. Molecular and functional hallmarks

AuthorsDocio, Inmaculada; Ramirez, Maria; Cáceres, Ana Isabel; Olea, Elena ; Gallego-Martin, Teresa ; Rocher, Asunción
Issue Date2016
Citation14th International Meeting of the European Calcium Society (2016)
AbstractAn important path of extracellular calcium influx in carotid body chemoreceptor cells (CBCC) during hypoxic activation and neurotransmitter release is through voltage activated calcium channels of the plasma membrane. Both high (HVA) and low voltage-activated (LVA) Ca2+ channels are present in CBCC, yet no much is known about the relevance of the LVA T-type channels. Three different genes codify for T-type channels, Cav3.1, Cav3.2 and Cav3.3, but only the Cav3.2 isoform has been found in carotid body. It has been reported that chronic hypoxia (CH) up-regulates Cav3.2 channel expression in PC12, chromaffin and pulmonary artery smooth muscle cells and, more recently, in CBCC. In the present study, we investigate the expression and the role of T-type Ca2+ channels in rat CB responses to acute and chronic hypoxia using a combination of pharmacological and molecular approaches. By immunocytochemistry and RT-PCR experiments we provide molecular evidence for a main presence of Cav3.1 and minor Cav3.2 expression, but not Cav3.3, in CBCC. Rats exposure to CH during 7 days up-regulates both, Cav3.1 and Cav3.2 channels, but mainly the former. Hypoxia stimulated CB response can be 50% reduced by specific T-type inhibitors: low concentration of mibefradil, Ni2+ and TTA-A2 and TTA-P2 blockers. We demonstrated augmented responses in CH treated rat CB which also are 50% sensitive to Ni2+ and mibefradil. We conclude that in rat CBCC, Cav3.1 is the predominant T-type calcium channel contributing to basal and CH augmented CBCC excitability and secretory response.
DescriptionResumen del póster presentado al 14th International Meeting of the European Calcium Society, celebrado en Valladolid (España) del 25 al 29 de septiembre de 2016.
Appears in Collections:(IBGM) Comunicaciones congresos
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