Hypertension (Dallas, Tex. : 1979) · 2026
β-Arrestin-2 Regulates Sodium Taste Processing.
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Grobe Connie C, Hamilton Autumn J, Treesukosol Yada, Grobe Justin L, Segar Jeffrey L, Sigmund Curt D
Аннотация
BACKGROUND: Altered detection and preference for sodium are associated with increased sodium intake, and increased sodium intake is associated with increased risk of hypertension. AT1R (angiotensin II type 1 receptor) second-messenger signaling is mediated and modulated by ARRB2 (β-arrestin-2), and both AT1R and ARRB2 in the brain influence sodium intake. Here, we examined the hypotheses that ARRB2 influences sodium taste hedonics and that these effects involve AT1R.
METHODS: Sodium intake behaviors and hedonic reactions of mice carrying a null mutation of the endogenous ARRB2 gene (Arrb2-KO [knockout] mice) were evaluated using 2-bottle choice testing, brief-access paradigms, and intraoral taste reactivity assays.
RESULTS: Arrb2-KO mice of both sexes exhibited dose-dependent increases in licking to sodium chloride and sucrose, but not quinine or citric acid, during a brief-access paradigm; rapid recovery of spontaneous isotonic saline intake after acute adulteration by quinine or exposure to hypertonic saline; persistently elevated isotonic saline intake even when dietary sodium content was increased from 0.15% to 1.00%; and reduced aversive reactions to acute intraoral isotonic saline. Finally, the spontaneous increase in isotonic saline intake by Arrb2-KO mice was abolished by administration of the AT1R antagonist losartan.
CONCLUSIONS: Together, these findings highlight a major role for ARRB2 in sodium taste processing, which appears to be mediated through an AT1R-dependent mechanism.
METHODS: Sodium intake behaviors and hedonic reactions of mice carrying a null mutation of the endogenous ARRB2 gene (Arrb2-KO [knockout] mice) were evaluated using 2-bottle choice testing, brief-access paradigms, and intraoral taste reactivity assays.
RESULTS: Arrb2-KO mice of both sexes exhibited dose-dependent increases in licking to sodium chloride and sucrose, but not quinine or citric acid, during a brief-access paradigm; rapid recovery of spontaneous isotonic saline intake after acute adulteration by quinine or exposure to hypertonic saline; persistently elevated isotonic saline intake even when dietary sodium content was increased from 0.15% to 1.00%; and reduced aversive reactions to acute intraoral isotonic saline. Finally, the spontaneous increase in isotonic saline intake by Arrb2-KO mice was abolished by administration of the AT1R antagonist losartan.
CONCLUSIONS: Together, these findings highlight a major role for ARRB2 in sodium taste processing, which appears to be mediated through an AT1R-dependent mechanism.