D. Villarreal et al., EFFECTS OF RENAL DENERVATION ON POSTPRANDIAL SODIUM-EXCRETION IN EXPERIMENTAL HEART-FAILURE, The American journal of physiology, 266(5), 1994, pp. 180001599-180001604
The hormonal, hemodynamic and renal excretory changes after an oral lo
ad of sodium were examined in renal-denervated dogs with an arterioven
ous (AV) fistula and the syndrome of compensated high-output heart fai
lure. After ingestion of a meal containing 125 meq of sodium, the tota
l postprandial urinary sodium excretion and fractional sodium excretio
n were approximately twofold higher in the renal-denervated AV fistula
dogs, compared with a control group with intact renal nerves (P < 0.0
5). The postprandial elevations in right atrial pressure, plasma atria
l natriuretic factor, and filtered load of sodium were similar in the
two groups (P > 0.05). Mean arterial pressure and plasma renin activit
y remained unchanged from baseline in the two subsets of animals (P >
0.05). In the renal-denervated AV fistula dogs, ingestion of a low-sal
t meal containing 2-3 meg 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 atri
al natriuretic factor were modest and inconsistent. These results demo
nstrate that the renal nerves play an important modulatory role for po
stprandial sodium metabolism after a high-salt meal in experimental co
mpensated high-output heart failure. It is suggested that the renal ne
rves attenuate the expression of postprandial natriuretic mechanisms v
ia a direct tubular mechanism of action.