Key Points
- To determine whether renal nerves are necessary for the development of salt appetite and compensatory hormone secretion following extracellular fluid depletion.
- Studied fluid intake and hormone secretion in intact and bilaterally renal-denervated rats following extracellular fluid depletion.
- Induced hypovolemia and mild hypotension via subcutaneous injections of furosemide (10 mg/kg) followed by captopril (5 mg/kg).
- Assessed intake of water and 0.3 M NaCl solution, total fluid balance, and plasma levels of renin, aldosterone, and angiotensin I.
- Renal-denervated rats drank significantly less 0.3 M NaCl solution and reached a significantly greater negative sodium and water balance compared with intact controls, despite consuming similar volumes of plain water.
- Renal denervation did not impair the secretion of renin and aldosterone, the generation of angiotensin I, or the excretion of water and sodium.
Structured PICO
Does bilateral renal denervation reduce salt appetite in rats following extracellular fluid depletion?
PPopulationRats subjected to extracellular fluid depletion (hypovolemia with mild hypotension) via subcutaneous injections of furosemide (10 mg/kg) and captopril (5 mg/kg)
IInterventionBilateral renal denervation
CComparatorIntact control rats
OOutcomeIngestion of water and 0.3 M NaCl solutionsurrogate
Bilateral renal denervation impairs sodium appetite in response to hypovolemia, indicating renal nerves are important for normal salt appetite elaboration.