RESUMO
Previous data from our laboratory have indicated that acute third ventricle injections of Zn2+ elicit a significant antidipsogenic response in rats in three different situations; dehydration, and central angiotensinergic or cholineric stimulation. In the present study we analyzed whether this response depends on voltage-dependent calcium channels. Dehydrated (14 h of water deprivation, overnight) animals received 2-microliters i.c.v. injections of zinc acetate (Zn(Ac)2; 300 pmol/rat) after pretreatment with the voltage-dependent calcium channel blockers gadolinium (Gd3+; 0.03, 3.0 and 30 pmol/rat) or verapamil (VER; 0.027, 0.05 and 0.11 pmol/rat). Both blockers reserved the antidipsogenic effect of third ventricle injections of Zn2+ in a dose-dependent manner. After 120 min, animals pretreated with saline receiving Zn(Ac)2 drank 3.10 +/- 0.57 ml/100 g body weight while those pretreated with Gd3+ at the highest dose displayed a water intake of 5.45 +/- 0.41 ml/100 body weight (P < 0.01). Animals pretreated with the vehicle of VER receiving Zn(Ac)2 drank 3.15 +/- 0.45 ml/100 g while animals pretreated with VER at the highest dose receiving Zn(Ac)2 drank 6.16 +/- 0.62 ml/100 g (P < 0.01). The antidipsogenic effect of Zn(Ac)2 seems to be specific since the metal (same dose and injection procedures) did not modify food intake in rats after 24 h of food deprivation. It is suggested that Zn2+ exerts its antidipsogenic effect by activation of mechanism(s) depending on the functional integrity of voltage-dependent calcium channels.
