EFFECT OF NA-LINE AND ANOXIA-INDUCED CATECHOLAMINE RELEASE FROM RAT CAROTID-BODY( AND K+ CHANNEL BLOCKADE ON BASE)

Ionic membrane currents are hypothesized to play a major role in deter mining secretion from carotid body glomus cells, and increased secreti on likely mediates the increase in nerve activity in response to hypox ia. The hypothesis that Na+ and K+ channels play an important role in determining secretion and nerve activity was tested by measuring singl e-fiber afferent nerve activity along with an estimate of free tissue catecholamine using Nafion-covered carbon-fiber microelectrodes placed in rat carotid bodies in vitro. Baseline and anoxia-stimulated (1 min duration; PO2 of similar to 0 Torr at nadir) levels were quantified. Sham treatment had no significant effect. Tetrodotoxin (2 mu m) ablate d the nerve activity and reduced peak catecholamine (19.5 +/- 3.1 to 1 4.5 +/- 3.4 mu M; P < 0.05). Cesium (10 mu m) had no effect on catecho lamine but reduced the nerve response (19.8 +/- 2.7 to 7.8 +/- 2.0 Hz; P < 0.05). 4-Aminopyridine (4 mM) significantly reduced the nerve res ponse (17.2 +/- 3.7 to 4.9 +/- 1.9 Hz; P < 0.05) and increased the bas eline (0.9 +/- 0.2 to 3.1 +/- 0.8 mu M; P < 0.05) and reduced the peak catecholamine (10.0 to 4.3 +/- 0.8 mu M; P < 0.05) levels. These resu lts demonstrate that Na+ and K+ channels play an important role in mod ulating the secretory and nerve responses. However, channel blockers d o not emulate severe hypoxia, suggesting that hypoxia transduction pre cedes, at least in part, through an alternate pathway.