Rhcg, also known as Rhesus C glycoprotein, is a key ammonia transporter. It plays a crucial role in urinary acid excretion, mainly expressed in the intercalated cells of the renal collecting duct [1,2]. In the kidney, it is involved in the process of ammonia secretion, which is essential for maintaining acid-base balance [2]. Genetic models, such as gene knockout mouse models, can be valuable for studying its function.

In in vivo experiments using C57BL/6J mice, aldosterone was found to regulate the membrane expression of Rhcg through the mineralocorticoid receptor and PKC pathways, with extracellular potassium level modulating this effect [1]. Deletion of RhCG in mice reduces renal ammonium secretion strongly, causes metabolic acidosis in acid-challenged mice, and impairs restoration of normal acid-base status, indicating its importance in maintaining acid-base balance in the body [2].

In conclusion, Rhcg is essential for ammonia transport and urinary acid excretion, playing a key role in maintaining acid-base balance in the body. Mouse models, especially Rhcg KO models, have provided valuable insights into its function in renal acid-base regulation, highlighting its significance in understanding related physiological processes and potential disease mechanisms.

References:

1. Eguchi, Koji, Izumi, Yuichiro, Yasuoka, Yukiko, Kuwabara, Takashige, Mukoyama, Masashi. . Regulation of Rhcg, an ammonia transporter, by aldosterone in the kidney. In The Journal of endocrinology, 249, 95-112. doi:10.1530/JOE-20-0267. https://pubmed.ncbi.nlm.nih.gov/33705345/

2. Wagner, Carsten A, Devuyst, Olivier, Belge, Hendrica, Bourgeois, Soline, Houillier, Pascal. 2010. The rhesus protein RhCG: a new perspective in ammonium transport and distal urinary acidification. In Kidney international, 79, 154-61. doi:10.1038/ki.2010.386. https://pubmed.ncbi.nlm.nih.gov/20927037/