Pereira, Daniela de Toledo Borba [UNESP]Nozaki, Priscila Nakada [UNESP]Menani, José Vanderlei [UNESP]Colombari, EduardoDe Luca, Laurival Antonio [UNESP]Schoorlemmer, Guus Hermanus Maria2015-12-072015-12-072003Pharmacology, Biochemistry, And Behavior, v. 76, n. 2, p. 275-283, 2003.0091-3057http://hdl.handle.net/11449/130845Both osmoreception and baroreception are thought to involve ion channels that are sensitive to changes in membrane stretch. We investigated the effect of a blocker of stretch-activated ion channels, the Gd3+ ion, on osmoregulatory and cardiovascular responses in the intact rat. Intracerebroventricular injection of 50-100 nmol Gd3+ reduced thirst induced by various treatments. Similar doses also reduced intake of saline induced by various treatments. Intracerebroventricular injection of 100 nmol Gd3+ transiently increased arterial pressure and reduced the pressor response to intracerebroventricular angiotensin II (Ang II). Systemic administration of Gd3+ failed to alter thirst, except for a high dose (270 micromol/kg) that induced illness. This high dose failed to prevent urinary hypertonicity and excretion of a load of hypertonic NaCl. Intravenous infusion of 270 micromol/kg of Gd3+ reduced blood pressure and pressure responses to intravenous phenylephrine, but did not reduce the baroreceptor reflex control of heart rate. We conclude that the effects of Gd3+ on thirst and on the cardiovascular system are probably not due to a direct effect of the drug on stretch-sensitive ion channels. Instead, many of the effects of Gd3+ were compatible with blockade of voltage-gated Ca2+ channels.275-283engStretch-sensitive ion channelsGadoliniumThirstSodium intakeOsmoreceptorsBaroreceptorsArtigo10.1016/j.pbb.2003.08.001Acesso restrito1023597870118105454445009242742614592679