Abstract
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 αENaC (epithelial sodium channel α-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.
Highlights
The renin-angiotensin system (RAS) is a major hormone system involved in body fluid and sodium homeostasis [1]
The expressions of renin, angiotensinogen, angiotensin-converting enzyme-1 (ACE1), and ACE2 mRNAs in the taste cells of B6 mice were examined by reverse transcription-polymerase chain reaction (RT-PCR)
We have demonstrated that the taste organ has three major components of the RAS, namely renin, angiotensinogen, and ACE1, which would enable Angiotensin II (AngII) to be produced locally in the taste buds
Summary
The renin-angiotensin system (RAS) is a major hormone system involved in body fluid and sodium homeostasis [1]. Angiotensin II (AngII), an octapeptide hormone, is the most powerful biologically active product of the RAS and plays important roles in the regulation of vascular tone, cardiac function, and renal sodium re-absorption. AngII is thought to be a potent stimulator of sodium appetite and preference. Intracerebroventricular or intravenous infusion of AngII in the rat produces dose-dependent salt appetite and stimulates sodium intake over a range of concentrations that are normally rejected [2,3]. The gustatory system provides critical information about the quality and nutritional value of food before it is ingested.
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