Enhanced increase of plasma sodium pump inhibitory activity to saline expansion in vagosympathectomized and anaesthetized dogs.

Abstract

To investigate whether plasma sodium pump inhibitory activity is controlled by cardiopulmonary and aortic baroreceptors, mean arterial pressure, right atrial pressure, sodium and water balances, plasma renin activity, plasma aldosterone concentration and plasma antinatriferic activity (PAA; plasma sodium pump inhibitory activity) were determined before, during and after Ringer volume expansion (10% of body wt) in anaesthetized dogs. Animals were studied with intact reflexes (CTR, n = 7) and after acute cervical bilateral vagosympathetic denervation (VGT, n = 8). With the exception of PAA, none of the parameters were different between groups before, during or after Ringer volume expansion. The PAA (microA cm-2) was similar for both groups before expansion and before either sham (CTR) or vagosympathectomy (VGT) was performed (CTR = 3.6 +/- 0.4 vs. VGT = 4.3 +/- 0.3). Compared to baseline, PAA at the end of the volume expansion phase increased in both groups (CTR = 6.1 +/- 0.8, P < 0.05; VGT = 9.1 +/- 0.7, P < 0.0005); however, this PAA value was significantly greater in the VGT group than in the CTR group (P < 0.01). At the end of the post-expansion phase, PAA levels returned toward baseline in both groups (CTR = 4.4 +/- 0.5 vs. VGT = 4.8 +/- 0.2; n.s. vs. baseline); however, this PAA value in the CTR group was not significantly different from its pak value. The present data confirm that PAA is increased in response to saline volume expansion, and suggest that PAA synthesis and/or release is under inhibitory vagosympathetic control during saline volume expansion.