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Anti-thirst and anti-diuresis responses have been observed in rats with 50 mg/os of L-dopa and L-methyl-dopa. When rats are given simultaneously either Fla-63, a beta-hydroxylase inhibitory drug, or phentolamine, an alpha-adrenergic blocking agent, the anti-thirst effect is changed in an opposite way; however, the last effect is not statistically significant. These data suggest that the anti-thirst effect observed in the present study could be related to a higher amount of catecholamines synthesized and to the consequent activation of the CNS alpha-adrenergic neuronal pathways. Methyldopa, with long lasting effects, can block the thirst induced by solid food up to the 9th hour. The opposite effect determined by both inhibitory agents indicates that the dopaminergic pathways play a leading role in the thirst regulation system. Furthermore, the alpha-adrenergic pathways seem to be devoided of anti-diuretic effect, since both the above mentioned inhibitory agents do not affect it.

The thirst mechanism by carbamylcholine and the possible interactions with the renin-angiotensin system have been investigated. Rats placed in metabolic cages in order to measure the drunk water and the emitted urine were used. Carbamylcholine has been injected together with captopril, an inhibitor of the enzyme converting angiotensin I into angiotensin II, and with propranolol, which blocks the renin beta-receptors respectively. When given in combination with these substances, the thirst by carbamylcholine was not reduced; this result does not favour the hypothesis of a role of the renin-angiotensin system. On the contrary, the thirst by carbamylcholine seems to be due to a vasomotor action. These results confirm the hypothesis that an unbalance between the blood circulating mass and the venous vessels underlies the regulation of the thirst.

A reduction of the thirst was observed one hour after intramuscolar injection of 0.3 mg/kg propranolol in the rat; this effect was not observed with higher doses. According to work hypotheses, small doses could act blocking renal beta-adrenergic receptors: the stopped renin emission reduces angiotensin production that is the basic factor of thirst. The AA hypothesize that the lack of the effect in response to higher doses of propranolol can be explained through a different action of this drug which antagonizes the first one.