VASOPRESSIN INCREASES GLOMERULAR-FILTRATION RATE IN CONSCIOUS RATS THROUGH ITS ANTIDIURETIC ACTION

To evaluate the possible influence of chronic alterations in urine con centrating activity (CA) on renal hemodynamics, adult male Sprague-Daw ley rats were submitted for 7 days to one of three different levels of CA. CA was either reduced by increasing water intake (mixing the food with a gel bringing 1.6 mL water per g food) (Low-CA), or increased b y chronic intraperitoneal infusion of 1-desamino 8-D-arginine vasopres sin (200 ng/day) (High-CA). Low-CA, High-CA, and control rats were hou sed in metabolic cages, ate the same quantity of dry food (the amount provided being slightly lower than the spontaneous intake), and had fr ee access to drinking wafer. The only difference between groups thus c oncerned the water intake-vasopressin axis. Radiolabeled (C-14)inulin was infused chronically by osmotic minipumps. Urine was collected duri ng Days 5, 6, and 7, and blood samples were taken for determination of plasma composition (P), absolute and fractional (FE) urinary excretio n, and clearance (C) of inulin, creatinine, urea, and main electrolyte s. This protocol produced mean 24-h urine osmolality (U-asm) ranging f rom 500 to 3500 mosmol/kg H2O without inducing any disturbance in body fluids or plasma osmolality (Pasm). Results show that GFR (Cinsulin) was markedly and positively correlated with U-asm (r = 0.798, P < 0.00 1) and free water reabsorption (r = 0.819, P < 0.001). For U-asm = 250 0 mosm/kg H2O. GFR was 47% higher than for U-asm = 500 mosm/kg H2O. C- creat underestimated GFR in High-CA and overestimated it in Low-CA. FE (urea) was inversely related to U-asm, as expected from the increased reabsorption known to occur at low urine flows. It is tentatively prop osed that the intrarenal recycling of urea, triggered by vasopressin a nd essential to the urinary concentrating mechanism, might influence G FR indirectly by modifying the composition of the tubular fluid at the macula densa and thus the Intensity of the tubuloglomerular feedback control of GFR. Even if this mechanism remains to be confirmed, this s tudy unequivocally demonstrates, in normal conscious rats, that the le vel of urinary concentrating activity has a major influence on basal G FR.