Caracterização e modulação das correntes de cálcio e potássio dependentes de voltagem em células quimiorreceptoras tipo I do corpo carotídeo de ratos adultos

Abstract

The type I cells of the adult rat carotid body are the primary peripheral chemoreceptors that sense alteration of pÜ2, pCÜ2 or [H+] and these in tum determine the action potential frequency in the sensory fibers of the carotid sinus nerve. This process involves influx of Ca2+ through voltage-dependent Ca2+ channels and subsequent release of dopamine and other neurotransmitters. This study has characterized the types and the properties of Ca2+ channels in the type I cells, and the effects of neurotransmitters and another endogenous substances upon them. The total voltage-dependent Ca2+ current recorded from chemoreceptor type I cells of the adult rat carotid body in 10 mM Ca2+ was activated around -40 mV, reached a maximum amplitude of -94 ± 4.5 pA, was half inactivated at a holding potential of -38 mV and completely blocked by 500 /íM Cd2+. Somatostatin and dopamine significantly inhibited the whole-cell Ca2+ current in type I cells. The currents were sustained throughout a 70 ms voltage step and were almost twice as large when Ba2+ was used as the charge carrier instead of Ca2+. The dihydropyridine agonist (+)202-791 increased the Ca2+ current amplitude by 106 ± 11% at a step potential of -18 mV. The dihydropyridine Ca2+-antagonist nimodipine decreased the Ca2+ current amplitude by 40 ± 5% at a holding potential of -80 mV and 74 ± 3% at a holding potential of -60 mV. The nimodipine-sensitive current had a maximum amplitude at a membrane potential of -12 mV. The co-Conotoxin GVIA blocked the whole-cell Ca2+ current by 40 ± 0.1% and the co-CgTx GVIA-sensitive current had a maximum amplitude at a membrane potential of +2 mV.