ANP and sodium excretion during acute baroreflex hypertension in conscious dogs.

The influence of an acute baroreflex hypertension elicited by common carotid occlusion (CCO) on plasma atrial natriuretic peptide (ANP) and renal sodium excretion was investigated in chronically instrumented, conscious foxhounds receiving a normal-sodium diet. CCO (n = 6) significantly increased mean arterial pressure (from 102 +/- 5 to 144 +/- 3 mmHg; P less than 0.01) and sodium excretion (from 82 +/- 10 to 133 +/- 9 mumol/min; P less than 0.05). No changes in plasma ANP and right atrial pressure were observed during the acute hypertension. In contrast, an acute 20% volume expansion (n = 7) corresponding to 1.8% of body weight raised right atrial pressure (from 1.3 +/- 1.2 to 5.8 +/- 1.2 cmH2O; P less than 0.01) and induced a sustained elevation of plasma ANP (from 39 +/- 8 to 67 +/- 16 pg/ml; P less than 0.05). The natriuresis in response to CCO was eliminated when renal perfusion pressure was regulated at the control level by a renal arterial cuff (n = 4); under these conditions, sodium excretion even tended to decrease during CCO (from 81 +/- 17 to 46 +/- 13 mumol/min; P less than 0.05). In conclusion, an increase in renal perfusion pressure and not an elevated ANP level is important in mediating the natriuresis during CCO in conscious dogs. These results imply that changes in plasma ANP are not essential for the induction and maintenance of a pressure natriuresis.