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We have previously demonstrated that acute third ventricle injections of both lead and cadmium prevent the dipsogenic response elicited by dehydration or by central injections of dipsogenic agents such as angiotensin II, carbachol and isoproterenol in rats. We have also shown that the antidipsogenic action of cadmium may be due, at least in part, to activation of thirst-inhibitory central serotonergic pathways. In the present paper we show that in Wistar male rats the antidipsogenic effect of both lead acetate (3.0 nmol/rat) and cadmium chloride (3.0 nmol/rat) may be partially dependent on the activation of brain opiatergic pathways since central injections of naloxone (82.5 nmol/rat), a non-selective opioid antagonist, blunt the thirst-inhibiting effect of these metals. One hundred and twenty minutes after the second third ventricle injections, dehydrated animals (14 h overnight) receiving saline + sodium acetate displayed a high water intake (7.90 +/- 0.47 ml/100 g body weight) whereas animals receiving saline + lead acetate drank 3.24 +/- 0.47 ml/100 g body weight. Animals receiving naloxone + lead acetate drank 6.94 +/- 0.60 ml/100 g body weight. Animals receiving saline + saline drank 8.16 +/- 0.66 ml/100 g body weight whilst animals receiving saline + cadmium chloride drank 1.63 +/- 0.37 ml/100 g body weight. Animals receiving naloxone + cadmium chloride drank 8.01 +/- 0.94 ml/100 g body weight. It is suggested that acute third ventricle injections of both lead and cadmium exert their antidipsogenic effect by activating thirst-inhibiting opioid pathways in the brain.

Opiatergic participation in the thirst-inhibiting effect of acute third ventricle injections of cadmium (Cd2+) and lead (Pb2+)