Interaction between cholinergic and adrenergic synapses of the rat subfornical organ and the thirst-inducing effect of angiotensin II.

Previous studies by our group and other authors have demonstrated that application of carbachol or angiotensin II to the subfornical organ (SFO) of satiated rats causes an intense thirst-inducing response. It has also been demonstrated that muscarinic cholinergic synapses are mainly involved in the thirst-inducing effect of carbachol, with a secondary role played by nicotinic receptors. The beta-adrenergic pathways of the SFO have also been shown to participate in the regulation of water intake. The present study was designed to investigate the possible interaction between cholinergic and adrenergic neurons of the subfornical organ and the effect of angiotensin II and carbachol in the regulation of water intake by this structure. The intense water intake induced by injection of 2 nmol carbachol into the SFO was markedly reduced when different doses of propranolol (20, 40, 80, and 160 nmol) were previously injected. The response to carbachol, however, was not changed by previous treatment with regitine (20, 40, and 80 nmol). Injection of 0.1 to 4.0 ng angiotensin II into the SFO caused a dose-dependent increase in water intake. When the 4 ng dose of angiotensin was injected into the SFO after an injection of atropine (20, 40, and 80 nmol), complete absence of water intake was observed, the same occurring when propranolol was previously injected at doses of 40 and 80 nmol. The thirst-inducing effect of angiotensin II (4 ng) was not changed by previous injection of hexamethonium (20, 40, 80, and 160 nmol) or phentolamine (20, 40, and 80 nmol). These results permit us to suggest that angiotensin II and carbachol induce thirst when applied to the SFO by acting through independent systems. The participation of beta-adrenergic receptors in the thirst-inducing effect of angiotensin II and carbachol was also demonstrated, as well as the participation of muscarinic cholinergic receptors in the thirst-inducing effect of angiotensin II injected into the SFO.