Effects of alpha 2 and beta 1-adrenergic blockers on thirst in rats

GAUNA, H. F.; BOSCH, P.; POLONI, L. A.

COMUNICACIONES BIOLOGICAS

Lugar: Buenos Aires; Año: 1996 vol. 14 p. 46 - 65

0326-1956

Experiments were conducted to examine the effects of a2-adrenergic antagonist yohimbine on primary thirst, hydrosaline renal excretion and the degree of participation of a2 and b1-adrenoreceptor on these functions. Male albino rats (Wistar) were used in all experiments. In Experiment 1, rats were exposed to osmotic thirst by 24 hr water deprivation, after which they received different doses of yohimbina hydrochloride (0.3, 0.6, 3.0 and 6.0 mg/Kg body wt ip). Yohimbine induced a significant dipsogenic effect only at 0.6-mg dose. In Experiment 2, the dipsogenic stimulus was a sc injection of NaCl hypertonic solution (hypovolemic thirst), after which animals received a single 0.3, 3.0 or 6.0-mg dose of yohimbine hydrochloride/Kg body wt ip. A significant thirst stimulation was observed for all doses assayed. However, the response was more effective at a 6-mg dose of yohimbine/kg body wt. In Experiment 3 renal-denervated rats with hypovolemic thirst received 6.0 mg of yohimbine hydrochloride/Kg body wt ip. Renal denervation partially blocked the dipsogenic effect of yohimbine. In Experiment 4 the effects of yohimbine (6.0 mg/Kg body wt ip), atenolol (2 mg/Kg body wt ip) and yohimbine prior to atenolol injection in hypertonic solution injected rats, were evaluated. Yohimbine increased water intake and urinary volume, effects which were partially reverted by atenolol. Moreover, yohimbine induced antinatriuresis and antikaliuresis as compared with atenolol. In Experiment 5 mean arterial pressure was determined by carotid artery catheterization. A significant decrease in this parameter after yohimbine injection (6.0 mg/Kg body wt ip) was observed as compared with the previous control period (saline solution of NaCl 0.9 %). We conclude that the hypotensive action of yohimbine partly accounts for increased water intake and that diuresis would not be secondary to the dipsogenic effect since there was no significant correlation between both parameters. The antinatriuretic effect of yohimbine would be secondary to a2-adrenergic proximal tubular reabsortion since yohimbine clocking presynaptic receptors could increase catecholamine release and simultaneously induce the diuretic and antinatriuretic effect.