The role of the cardiac nerves in the regulation of sodium excretion in conscious dogs

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Abstract
Conscious, chronically instrumented dogs, maintained on a high sodium intake, were used to investigate whether surgical cardiac denervation impairs the natriuresis associated with left atrial pressure increase produced in three ways: during an increase in left atrial pressure by means of a reversible mitral stenosis (protocol 1); after an i.v. saline load (1.0 ml 0.9%·saline min−1·kg−1 over 60 min) (protocol 2); after an oral saline load (14.5 mmol Na·kg−1 given with the food as an isotonic solution) (protocol 3). During a reversible mitral stenosis, in intact dogs, urine volume and sodium excretion increased markedly (from 34–145 μl·min−1·kg−1 and from 3–12 μmol·min−1·kg−1); mean arterial pressure increased by an average of 2 kPa (15 mm Hg) and heart rate by 55 b/min; plasma renin activity fell from 0.37–0.21 ng Al·ml−1·h−1. Cardiac denervation eliminated these effects of left atrial distension except for a small increase in heart rate (12 b/min). This indicates that the natriuresis and diuresis during left atrial distension resulted from stimulation of receptors located in the left atrium. In contrast, during protocol 2 and 3, the same amounts of sodium and water were excreted in the cardiac denervated dogs as compared to the intact dogs. A comparable decrease in plasma renin activity also was observed. — Apparently the presence of the cardiac nerves is not a prerequisite for maintenance of sodium and water homeostasis.