INFLUENCE OF THE RENAL NERVES ON SODIUM-EXCRETION DURING PROGRESSIVE REDUCTIONS IN CARDIAC-OUTPUT

The purpose of this study was to elucidate the role of the renal nerve s in promoting sodium retention during chronic reductions in cardiac o utput. In five dogs, the left kidney was denervated and the urinary bl adder was surgically divided to allow separate 24-h urine collection f rom the innervated and denervated kidneys. Additionally, progressive r eductions in cardiac output were achieved by employing an externally a djustable occluder around the pulmonary artery and by servo-controllin g right atrial pressure (control = 0.9 +/- 0.2 mmHg) at 4.7 +/- 0.1, 7 .5 +/- 0.1, and 9.8 +/- 0.2 mmHg for 3 days at each level. At the high est level of right atrial pressure, the 24-h values for mean arterial pressure (control = 97 +/- 3 mmHg) and cardiac output (control = 2,434 +/- 177 ml/min) were reduced similar to 25 and 55%, respectively; glo merular filtration rate fell by similar to 35% and renal plasma flow b y similar to 65%. However, despite the sodium retention induced by the se hemodynamic changes, there were no significant differences in renal hemodynamics or sodium excretion between the two kidneys during pulmo nary artery constriction. In contrast, after release of the pulmonary artery oceluder on day 9, sodium excretion increased more (similar to 28% during the initial 24 h) in innervated than in denervated kidneys. These results suggest that the renal nerves are relatively unimportan t in promoting sodium retention in this model of low cardiac output bu t contribute significantly to the short-term elimination of sodium aft er partial restoration of cardiac output and mean arterial pressure.