AJP - Regulatory, Integrative and Comparative Physiology, Vol 256, Issue 5 1044-R1049, Copyright © 1989 by American Physiological Society
ANP and sodium excretion during acute baroreflex hypertension in conscious dogs
H. Ehmke, P. Persson, U. Kogler, R. Lang and H. Kirchheim
I. Physiologisches Institut, Universitat Heidelberg, Federal Republic of Germany.
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.
