M. Heringlake, J. Sehested, L. Bahlmann, H. Paarmann, H. Groesdonk, S. Klaus, H. Pagel
[Applied Cardiopulmonary Pathophysiology 15: 24-28, 2011]
Controversial results regarding the role of vasopressin as a mediator of ethanol-induced diuresis raise the question, whether ethanol may stimulate diuresis directly on the level of the kidney, possibly by its vasodilating properties. We thus studied the effects of different ethanol-concentrations (0.5 ‰, 1 ‰, 2 ‰, and 4 ‰; n = 4 to 6, respectively) – in the presence of 10 mU/l vasopressin in the perfusion medium – and the effect of absence of vasopressin (-VP; n = 5) in isolated rat kidneys perfused for 180 minutes in a closed circuit system. A control group (con+VP; n = 6) was studied with the standard perfusion medium containing 10 mU/l vasopressin. Urine flow (UV) and free water clearance (CH2O) were increased (UV: con+VP: 124 ± 78 vs. –VP: 258 ± 88 ml*min-1*g kidney-1; CH2O: - con+VP: 20.4 ± 7.4 vs. –VP: 51.6 ± 20.8 ml*min-1*g kidney-1, p < 0.05 respectively) and fractional reabsorption of sodium (FRNa) were increased in rats perfused without vasopressin (FRNa: con+VP: 83.7 ± 8.3 vs. –VP: 75.0 ± 2.6 %, p < 0.05). Ethanol-treatment had no effect on urine flow, sodium and potassium excretion, glomerular filtration rate, and renal vascular resistance. These data show that ethanol-mediated diuresis cannot be explained by intrinsic effects of ethanol on the kidney, at least in an isolated and denervated perfused rat kidney model.
Key words: ethanol-induced diuresis, fluid homeostasis, renal function
Matthias Heringlake, M.D.
Klinik für Anaesthesiologie
Universität zu Lübeck
Ratzeburger Allee 160