CP O'Donnell, AR Schwartz, PL Smith, JL Robotham, RS Fitzgerald and M Shirahata
Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University, Baltimore, Maryland, USA.

The purpose of this study was to examine the role of afferent input in the reflex modulation of renal sympathetic nerve activity (SNA) in response to apnea. Apneas of 20-, 40-, and 60-s duration were induced in the anesthetized, paralyzed cat (n = 7) ventilated with either room air 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 (Pa) of 9 +/- 3, 30 +/- 9, and 45 +/- 12 mm 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, at a matched level of PaCO2, by at least 80%, and to eliminate any increase in Pa. During the first breath of the postapneic period, there was a partial inhibition of renal SNA. During the second and third breaths of the postapneic period, there was a marked fall in renal SNA that was associated with a precipitous decline in directly recorded carotid 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 inputs from thoracic afferents and arterial baroreceptors likely contributing to the marked inhibition of renal SNA immediately after the apnea.

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