Expression of Renin-Angiotensin System Components in the Taste Organ of Mice

Expression of Renin-Angiotensin System Components in the Taste Organ of Mice
复制标题

DOI:
10.3390/nu11092251
复制
发表时间:
2019-09-01
期刊:
影响因子:
5.9
通讯作者:
Ninomiya, Yuzo
Ninomiya, Yuzo
中科院分区:
医学2区
文献类型:
--
作者:
Shigemura, Noriatsu;Takai, Shingo;Ninomiya, Yuzo

文献摘要

被引文献

相似文献

系统性的肾素-血管紧张素系统(RAS)是体液和钠稳态的重要调节器。血管紧张素II(AngII)是RAS的关键活性产物。我们以前发现,循环血管紧张素II抑制阿米洛利敏感的盐的味觉反应,并通过在味觉细胞中表达的血管紧张素II 1型受体(AT 1)增强对甜味化合物的反应。然而,由AngII调制味觉功能的分子机制仍不清楚。在这里,我们研究了三个RAS组件,即肾素,血管紧张素原,血管紧张素转换酶-1(ACE 1),在小鼠味觉组织的表达。我们发现,所有这三种RAS成分都存在于菌状和轮廓状乳头的味蕾中,并与α ENaC(上皮钠通道α亚基,盐味觉受体)或T1 R3(味觉受体1型成员3,甜味受体成分)共表达。缺水小鼠味觉细胞中的肾素表达水平显著增加(p < 0.05)。这些结果表明,味觉器官中存在局部RAS,并表明味觉功能可能受局部产生和循环AngII的调节。血管紧张素II对外周味觉敏感性的这种综合调节可能在钠/热量稳态中发挥重要作用。
The systemic renin-angiotensin system (RAS) is an important regulator of body fluid and sodium homeostasis. Angiotensin II (AngII) is a key active product of the RAS. We previously revealed that circulating AngII suppresses amiloride-sensitive salt taste responses and enhances the responses to sweet compounds via the AngII type 1 receptor (AT1) expressed in taste cells. However, the molecular mechanisms underlying the modulation of taste function by AngII remain uncharacterized. Here we examined the expression of three RAS components, namely renin, angiotensinogen, and angiotensin-converting enzyme-1 (ACE1), in mouse taste tissues. We found that all three RAS components were present in the taste buds of fungiform and circumvallate papillae and co-expressed with alpha ENaC (epithelial sodium channel alpha-subunit, a salt taste receptor) or T1R3 (taste receptor type 1 member 3, a sweet taste receptor component). Water-deprived mice exhibited significantly increased levels of renin expression in taste cells (p < 0.05). These results indicate the existence of a local RAS in the taste organ and suggest that taste function may be regulated by both locally-produced and circulating AngII. Such integrated modulation of peripheral taste sensitivity by AngII may play an important role in sodium/calorie homeostasis.