Renal Denervation Eliminates the Renal Response to Continuous Positive-Pressure Ventilation

Elevation of the expiratory pressure during mechanical ventilation is frequently associated with a decrease in urine flow and electrolyte excretion (1-3). Although major emphasis has been placed on intrathoracic volume receptors and antidiuretic hormone (4, 5), until recently, very little definitive information concerning the mechanism of the reflex antidiuresis associated with continuous positive pressure ventilation (CPPV) has been reported. In a previous study, we demonstrated that selective denervation of the aortic arch and carotid sinus baroreceptors eliminated the renal response to CPPV using a positive end expiratory pressure (PEEP) of 10 cm H20; in contrast, bilateral cervical vagotomy did not alter the antidiuresis or antinatriuresis observed during CPPV (6). This is in accordance with the earlier work of Baratz et al. (7) and Tarak and Chaudhury (8) and provides additional evidence that cardiopulmonary receptors, whose afferent nerve fibers are in the vagi, do not initiate this response. Tarak and Chaudhury (8) have also reported that CPPV can cause suppression of urine flow without elevated levels of antidiuretic hormone. One possible explanation for the arterial baroreceptor mediated antidiuresis and antinatriuresis associated with CPPV may be related to an alteration in renal nerve activity. It is well documented that the carotid sinus and aortic arch baroreceptors participate in controlling renal nerve activity. Kezdi and Geller (9) have demonstrated that an inverse relation exists between carotid sinus pressure and renal sympathetic nervous discharge and that this relation is essentially linear over the