REFLEX STIMULATION OF RENAL SYMPATHETIC-NERVE ACTIVITY AND BLOOD-PRESSURE IN RESPONSE TO APNEA

The purpose of this study was to examine the role of afferent input in the reflex modulation of renal sympathetic nerve activity (SNA) in re sponse to apnea. Apneas of 20-, 40-, and 60-s duration were induced in the anesthetized, paralyzed cat (n = 7) ventilated with either room a ir or 100% oxygen. While receiving room air, there were increases (p < 0.005) in renal SNA of 34.5 +/- 4.2%, 53.3 +/- 6.4%, and 59.9 +/- 7.2 % of maximum during the 20-, 40-, and 60-s apneas, respectively. There were corresponding increases (p < 0.025) in mean arterial pressure (P al of 9 +/- 3, 30 +/- 9, and 45 +/- 12 man Hg during the 20-, 40-, and 60-s apneas while receiving room air, respectively. The effect of 100 % oxygen was to reduce (p < 0.0001) the renal SNA response to apnea, a t a matched level of Pa-co2, by at least 80%, and to eliminate any inc rease in Pa. During the first breath of the postapneic period, there w as a partial inhibition of renal SNA. During the second and third brea ths of the postapneic period, there was a marked fall in renal SNA tha t was associated with a precipitous decline in directly recorded carot id chemoreceptor activity (n = 2). The magnitude of the fall in renal SNA after apnea was related to the degree of postapneic hypertension. We conclude that hypoxic chemoreceptor stimulation is the predominant factor generating the renal SNA response to apnea, with modulating inp uts from thoracic afferents and arterial baroreceptors likely contribu ting to the marked inhibition of renal SNA immediately after the apnea .