Effect of Vasopressin V1a Receptor Blockade on Renal Osmoregulatory Function in L-Thyroxine-Induced Hyperthyroid Rats with Different Blood Vasopressin Levels

The effect of V 1a receptor (V 1a R) blockade on the renal osmoregulatory function was studied in WAG and Brattleboro rats under L-thyroxin-induced hyperthyroidism. In both rat strains, hyperthyroidism promoted the development of a diuretic response due to an increase in glomerular filtration rate. In vasopressin-deficient Brattleboro rats, in contrast to the WAG strain, an increase in urinary flow rate was due to a decrease in solute-free water reabsorption relative to control. The direction of changes in the renal natriuretic function during L-thyroxine intake was determined by endogenous vasopressin levels: while hyperthyroid WAG rats showed a natriuretic response, vasopressin-deficient Brattleboro rats developed antinatriuresis due to a direct stimulatory effect of thyroid hormones on sodium reabsorption. The inhibition of sodium reabsorption in hyperthyroid WAG rats was abolished by V 1a R blockade. It is assumed that V 1a R stimulation plays a key role in the inhibition of sodium reabsorption under L-thyroxine-induced hyperthyroidism, while the direct vasopressin-independent effect of the thyroid hormones is aimed at the activation of sodium transport and suppression of water reabsorption.