EFFECTS OF RENAL DENERVATION ON POSTPRANDIAL SODIUM-EXCRETION IN EXPERIMENTAL HEART-FAILURE

Citation
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
Citations number
26
Categorie Soggetti
Physiology
ISSN journal
00029513
Volume
266
Issue
5
Year of publication
1994
Part
2
Pages
180001599 - 180001604
Database
ISI
SICI code
0002-9513(1994)266:5<180001599:EORDOP>2.0.ZU;2-7
Abstract
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.