Angiotensin II Modulates Salty and Sweet Taste Sensitivities
Angiotensin II Modulates Salty and Sweet Taste Sensitivities
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DOI：
10.1523/jneurosci.5599-12.2013
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发表时间：
2013-04-10
影响因子：
5.3
通讯作者：
Ninomiya, Yuzo
中科院分区：
文献类型：
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作者：
Shigemura, Noriatsu;Iwata, Shusuke;Ninomiya, Yuzo
了解饮食钠的味觉检测机制对高血压的预防和治疗具有重要意义。在这里，我们表明血管紧张素II (AngII)，体液和钠稳态的主要介质，调节咸味和甜味的敏感性，并且这种调节严重影响小鼠的摄食行为。味觉神经记录显示，AngII抑制了盐对阿米洛利敏感的味觉反应。令人惊讶的是，AngII也增强了神经对甜味剂的反应，但对KCl、酸、苦或抗抗剂的反应没有影响。AngII对神经反应的这些影响被血管紧张素II 1型受体（AT1）拮抗剂CV11974阻断。在行为学测试中，CV11974治疗降低了血浆AngII水平升高的饮水受限小鼠对NaCl和甜味剂的高舔食率。在味觉细胞中，AT1蛋白与ENaC（上皮钠通道α亚基，一种对阿米洛胺敏感的盐味受体）或T1r3（一种甜味受体成分）共表达。这些结果表明味觉器官是AngII的外周靶点。AngII对阿米洛利盐味敏感性的特异性降低可能与钠摄入量增加有关。此外，AngII可能通过增强甜味反应来增加能量摄入。通过AngII信号，咸味和甜味偏好之间的联系可能会优化钠和卡路里的摄入量。
Understanding the mechanisms underlying gustatory detection of dietary sodium is important for the prevention and treatment of hypertension. Here, we show that Angiotensin II (AngII), a major mediator of body fluid and sodium homeostasis, modulates salty and sweet taste sensitivities, and that this modulation critically influences ingestive behaviors in mice. Gustatory nerve recording demonstrated that AngII suppressed amiloride-sensitive taste responses to NaCl. Surprisingly, AngII also enhanced nerve responses to sweeteners, but had no effect on responses to KCl, sour, bitter, or umamitastants. These effects of AngII on nerve responses were blocked by the angiotensin II type 1 receptor (AT1) antagonist CV11974. In behavioral tests, CV11974 treatment reduced the stimulated high licking rate to NaCl and sweeteners in water-restricted mice with elevated plasma AngII levels. In taste cells AT1 proteins were coexpressed with alpha ENaC (epithelial sodium channel alpha-subunit, an amiloride-sensitive salt taste receptor) or T1r3 (a sweet taste receptor component). These results suggest that the taste organ is a peripheral target of AngII. The specific reduction of amiloride-sensitive salt taste sensitivity by AngII may contribute to increased sodium intake. Furthermore, AngII may contribute to increased energy intake by enhancing sweet responses. The linkage between salty and sweet preferences via AngII signaling may optimize sodium and calorie intakes.