Bilateral renal denervation restored the impaired renal excretory response to an acute isotonic saline load in rats with edema-forming states compared to control rats.
Does bilateral renal denervation improve renal sodium and water excretion in rat models of edema-forming states?
Bilateral renal denervation restores normal renal sodium and water excretion in rat models of edema-forming states, suggesting that impaired excretion is partially dependent on increased basal efferent renal sympathetic nerve activity.
To define the role of the renal nerves in renal sodium-retaining edema-forming states, experiments were conducted in conscious chronically instrumented rats with congestive heart failure (myocardial infarction), nephrotic syndrome (adriamycin injection), and hepatic cirrhosis (common bile duct ligation). In each experimental model, renal excretion, as water or sodium, of an acutely administered oral or intravenous isotonic saline load was significantly less than that in control rats. Bilateral renal denervation of the experimental rats restored their renal excretory response to that of the control rats. In addition, in response to the acute administration of a standard intravenous isotonic saline load, the decrease in efferent renal sympathetic nerve activity was significantly less in all three experimental models compared with that of control rats. These results suggest that the impaired ability to excrete an acute isotonic saline load in these experimental models is partially dependent on an increase in basal efferent renal sympathetic nerve activity that fails to suppress normally in response to the isotonic saline load.
DiBona et al. (Wed,) conducted a other in Edema-forming states (congestive heart failure, nephrotic syndrome, hepatic cirrhosis). Bilateral renal denervation vs. Control rats was evaluated on Renal excretion of water or sodium in response to an acute isotonic saline load. Bilateral renal denervation restored the impaired renal excretory response to an acute isotonic saline load in rats with edema-forming states compared to control rats.