CHEMOTRANSDUCTION BY CAROTID-BODY CHEMORECEPTORS IS DEPENDENT ON BICARBONATE CURRENTS

Previous studies have demonstrated that bicarbonate enhances the speed and magnitude of the carotid body chemoreceptor response to hypoxia. We hypothesized that this enhancement is associated with enhanced hypo xia-induced catecholamine (CAT) secretion from glomus cells. Single-fi ber nerve activity and free tissue catecholamine (carbon fiber microvo ltammetry) were measured in rat carotid body, in vitro. The peak CAT a nd nerve responses during 1 min anoxia were larger in the presence of bicarbonate than in its absence (peak CAT: 16.7 +/- 2.7 vs. 5.1 +/- 1. 1 mu M; peak nerve: 28.2 +/- 1.6 vs. 16.7 +/- 1.4 Hz). Bicarbonate par ticularly enhanced the responses to moderate hypoxia (P-O2 similar to 80 Torr) which caused no secretion or increased nerve activity in the absence of bicarbonate, but caused significant stimulation in the pres ence of bicarbonate (peak nerve = 15.2 Hz; peak CAT = 8.6 mu M). The b icarbonate effect was not due to alterations in intracellular pH since it was not blocked by exchanger blockers (DIDS) or mimicked by acidif ication of the medium. However, anion channel blockade by 9-AC or DPC reduced anoxia-induced CAT secretion in the presence of bicarbonate. W e conclude that bicarbonate greatly enhances stimulus/secretion coupli ng in glomus cells, probably through modulation of an anion current ca rried by bicarbonate. (C) 1998 Elsevier Science B.V. All rights reserv ed.