1: Am J Physiol. 1994 May;266(5 Pt 2):R1599-604. 

Effects of renal denervation on postprandial sodium excretion in experimental
heart failure.

Villarreal D, Freeman RH, Johnson RA, Simmons JC.

Department of Physiology, University of Missouri School of Medicine, Columbia
65212.

The hormonal, hemodynamic and renal excretory changes after an oral load of
sodium were examined in renal-denervated dogs with an arteriovenous (AV) fistula
and the syndrome of compensated high-output heart failure. After ingestion of a
meal containing 125 meq of sodium, the total postprandial urinary sodium
excretion and fractional sodium excretion were approximately twofold higher in
the renal-denervated AV fistula dogs, compared with a control group with intact
renal nerves (P < 0.05). The postprandial elevations in right atrial pressure,
plasma atrial natriuretic factor, and filtered load of sodium were similar in
the two groups (P > 0.05). Mean arterial pressure and plasma renin activity
remained unchanged from baseline in the two subsets of animals (P > 0.05). In
the renal-denervated AV fistula dogs, ingestion of a low-salt meal containing
2-3 meq of sodium produced elevations in creatinine clearance and filtered load
of sodium of similar magnitude to the high-salt meal. However, the increases in
sodium excretion and plasma atrial natriuretic factor were modest and
inconsistent. These results demonstrate that the renal nerves play an important
modulatory role for postprandial sodium metabolism after a high-salt meal in
experimental compensated high-output heart failure. It is suggested that the
renal nerves attenuate the expression of postprandial natriuretic mechanisms via
a direct tubular mechanism of action.

PMID: 8203638 [PubMed - indexed for MEDLINE]