The aim of this study was to examine the contribution of the renal nerves to the sodium retention in chronic congestive heart failure produced by rapid ventricular pacing. In 10 female dogs the left kidney was denervated and the urinary bladder was split to allow separate 24-h urine collection from an innervated and a denervated kidney in the same dog. The dogs were placed on an 80-meq/day sodium intake and permitted to recover for at least 2 wk. Control measurements were made for 5 days followed by ventricular pacing at 270-300 beats/min for 6 days. Cardiac output (CO), measured with an electromagnetic flow probe around the ascending aorta, fell from a control of 2.4 +/- 0.3 to 1.4 +/- 0.2 l/min (6 day average) during pacing while mean arterial pressure (MAP) fell from 91 +/- 4 to 71 +/- 3 mmHg. In six dogs, sodium excretion fell to an average of less than 2 meq/day (80 meq/day intake) during the 6-day pacing period in both the innervated and denervated kidneys. In four dogs, sodium excretion returned back toward control on days 3-6 of pacing despite sustained reductions in CO and MAP. However, there were no differences in renal hemodynamics or electrolyte excretion between innervated and denervated kidneys in either the compensated or decompensated dogs. These results suggest that other control mechanisms, besides the renal nerves, are primarily responsible for the sodium retention in this model of chronic congestive heart failure.
Beta-adrenergic receptor-G protein-adenylate cyclase complex in experimental canine congestive heart failure produced by rapid ventricular pacing.
