Recently, the H+-activated G-protein coupled receptor OGR1 has been identified as a H+-sensor; its stimulation causes IP3 production and an increase in intracellular Ca2+. However no information is available concerning its functional and physiological role. Here we tested for a potential role of OGR1 in acid-base and electrolyte homeostasis. qRT-PCR and immunohistochemistry showed basolateral expression of OGR1 in several renal nephron segments. Intracellular pH measurements demonstrated that OGR1 stimulates Na+/H+-exchanger NHE3 in transfected HEK293B cells. The analysis of OGR1 KO mice did not show any changes in systemic acid-base status or renal acid excretion under normal conditions or after an acid load with NH4Cl for 24 hrs. However, OGR1 KO mice showed lower Mg2+ and Ca2+ excretion in urine on a normal diet. When animals were switched to a low Ca2+ diet (0.05 %), the KO mice showed higher urinary excretion with lower excretion of K+, Na+, and Mg2+. qRT-PCR demonstrated increased expression of TRPM6 (Mg2+ channel). The abundance of TRPV5, the major Ca2+ channel was unchanged. Our experiments suggest that OGR1 may be involved in the regulation of mineral balance.