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Role of Rh C Glycoprotein (Rhcg) in the Renal Response to Hypokalemia

Rh C Glycoprotein (Rhcg) is an NH3 transporter that is necessary for basal and acidosis‐stimulated renal ammonia excretion. Hypokalemia is an important cause of increased renal ammonia excretion. In the present studies we examined Rhcg's role in hypokalemia‐stimulated ammonia excretion. We used mice with collecting duct‐specific Rhcg deletion (CD‐Rhcg‐KO) generated using loxP‐Cre techniques; control (C) mice were Cre negative. Mice were pair‐fed K+‐free diet for 3 or 12 days. K+‐restriction caused urinary alkalinization, increased urine volume, increased ammonia excretion, and decreased potassium excretion. Similar to metabolic acidosis, hypokalemia increased Rhcg expression in the cortex and outer medulla in C mice, but there were no significant differences in urine ammonia, pH, volume or K+ between CD‐Rhcg‐KO and C mice. There were also no significant differences in Rhbg, H+‐ATPase or PEPCK expression or creatinine clearance between C and CD‐Rhcg‐KO mice after 12 days of K+‐free diet. Thus, in contrast to the necessity for CD Rhcg expression in the renal ammonia response to metabolic acidosis, CD Rhcg expression is not necessary for the increased urinary ammonia excretion that occurs in response to hypokalemia. We conclude that Rhcg's role in renal ammonia excretion varies in different models of increased ammonia excretion.