1: Am J Physiol. 1993 Apr;264(4 Pt 2):H1187-93. 

Neurohumoral modulators and sodium balance in experimental heart failure.

Villarreal D, Freeman RH, Johnson RA.

Department of Physiology, University of Missouri School of Medicine, Columbia.

The acute and chronic interactions of the renal nerves, atrial natriuretic
factor (ANF), and mineralocorticoids for the regulation of sodium balance were
examined in dogs with an arteriovenous (AV) fistula and the syndrome of
high-output heart failure (HOHF) (n = 6). After the AV fistula and bilateral
renal denervation, the animals avidly retained sodium for 5-7 days and then
regained sodium balance for the subsequent 3 wk. This compensation was
associated with the sustained elevations of plasma ANF and the normalization of
plasma renin. Subsequent administration of deoxycorticosterone acetate (DOCA)
for 10 days produced consistent sodium retention despite additional elevations
in plasma ANF. All of these responses were similar to previous studies in AV
fistula dogs with intact renal nerves. In a separate part of the study, the
renal actions of acute synthetic ANF infusions were examined in these
renal-denervated AV fistula dogs before and after DOCA. In the pre-DOCA
experiments, ANF infusions at 15, 30, and 100 ng.kg-1.min-1 produced
dose-related increases in urinary sodium excretion and significant elevations in
creatinine clearance. In the presence of DOCA, urinary sodium excretion was
markedly attenuated during identical ANF infusions. The composite results
suggest that mineralocorticoids have an important modulatory role for the
regulation of sodium balance in experimental HOHF. However, compared with
earlier studies in compensated AV fistula dogs with intact renal nerves, the
present studies demonstrate that blockade of efferent renal sympathetic nerve
activity can restore the natriuretic expression of acute elevations in
circulating ANF.

PMID: 8097382 [PubMed - indexed for MEDLINE]