AT1 receptors are widely distributed throughout the body, including vascular smooth muscle, kidney, heart and brain, which are responsible for mediating vasoconstriction and sodium re-absorption. The AT2 receptors are generally thought to oppose the actions of AT1 [47]. We hypothesized that if these receptors would be expressed in peripheral taste cells, circulating ANG II may act as a suppressive modulator for amiloride-sensitive salt responses. The reciprocal regulation by ANG II and enhancers (e.g. ALDO) on the peripheral salt taste sensitivity would contribute to their opposing actions on sodium intake and play Ruxolitinib an important role in sodium homeostasis. To explore this hypothesis,

we investigated gustatory nerve and behavioral responses to taste stimuli after administration of ANG II in mice and the expression of ANG II receptors in taste tissues [48]. Salty taste responses are composed of amiloride-sensitive and -insensitive components as mentioned above [17], [18] and [19]. Thus, the CT nerve responses in B6 mice were examined, because both amiloride-sensitive and -insensitive responses were involved. The CT nerve responses of B6 mice to NaCl started to decrease approximately 5 min after an intraperitoneal (i.p.) injection of ANG II, then reached near maximum suppression click here (∼70% of control

before ANG II) approximately 30 min after the injection. Recovery of the responses to near control levels took more than an hour after the injection. In contrast, ANG II had no such effect on responses to NaCl in the presence of 30 μM amiloride. Thus, most of the effect of ANG II was on amiloride-sensitive salt responses. Verteporfin The effect of ANG II on the taste responses was dose dependent and saturated at ∼1000 ng/kg bodyweight ANG II. Surprisingly, ANG II also enhanced nerve responses to sweeteners (natural sugars; glucose, sucrose, artificial sweetener; saccharin, SC45647),

but not to KCl, sour (HCl), bitter (quinine hydrochloride: QHCl) or umami (monosodium glutamate: MSG) tastants. These effects of ANG II on nerve responses were blocked by pretreatment of a specific antagonist of AT1, CV11974 [49]. These results indicate that ANG II acts on the peripheral taste organs via AT1, and modulates the CT nerve responses to sodium (amiloride-sensitive) and sweeteners selectively in mice [48]. Interestingly, significant increases of amiloride-sensitive CT nerve responses to NaCl were observed at 90–120 min after the ANG II administration. ALDO is stimulated by ANG II, and has been proposed as an enhancer of amiloride-sensitive salt taste responses in a time course of hours [25], [34], [35], [36], [37] and [38], illustrating that the increased amiloride-sensitive salt responses at 90–120 min may be mediated by endogenous ALDO stimulated by the exogenous ANG II infusion.