CHEMORECEPTOR NERVE EXCITATION MAY NOT BE PROPORTIONAL TO CATECHOLAMINE SECRETION

Enhanced catecholamine secretion from the carotid body glomus cells is hypothesized to play an essential role in mediating the peripheral ch emoreceptor response to hypoxia. To test aspects of this hypothesis, t he relationship between catecholamine secretion and nerve activity was examined during repetitive hypoxia stimuli and after catecholamine de pletion with reserpine. Single-fiber afferent nerve activity was measu red along with an estimate of free tissue catecholamine by using Nafio n-coated carbon-fiber microelectrodes placed in rat carotid bodies in vitro. Baseline and stimulated nerve and catecholamine levels were qua ntified during repetitive stimulation (anoxia of 1-min duration; Po-2 = 0 Torr at nadir, repeated each 200 s). Peak stimulated catecholamine progressively decreased from 26.4 +/- 2.6 mu M for the first stimulus to 7.5 +/- 0.9 mu M for the fifth stimulus (n = 15), but peak nerve a ctivity was much less affected (23.0 +/- 1.9 Hz, first trial; 19.9 +/- 1.4 Hz, fifth trial). An exposure to moderate hypoxia (similar to 80 Torr) before the repetitive anoxia stimuli produced catecholamine leve ls comparable to those obtained during repetitive anoxia, but peak ner ve activity was significantly less (22.5 +/- 3.4 Vs. 12.7 +/- 2.1 Hz). Pretreatment with reserpine (1 mg/100 g) resulted in a large reductio n in the average hypoxia-induced catecholamine response (1.4 +/- 0.3 m u M, n = 9), but peak, nerve activity was not different from nontreate d controls. These results demonstrate an independence between carotid body catecholamine secretion and nerve activity, suggesting that nerve excitation is, at least, partially mediated through pathways independ ent of granule secretion.