| First Author | Greenlee MM | Year | 2011 |
| Journal | J Am Soc Nephrol | Volume | 22 |
| Issue | 1 | Pages | 49-58 |
| PubMed ID | 21164026 | Mgi Jnum | J:185882 |
| Mgi Id | MGI:5430457 | Doi | 10.1681/ASN.2010030311 |
| Citation | Greenlee MM, et al. (2011) Mineralocorticoids stimulate the activity and expression of renal H+,K+-ATPases. J Am Soc Nephrol 22(1):49-58 |
| abstractText | In the renal collecting duct, mineralocorticoids drive Na(+) reabsorption, K(+) secretion, and H(+) secretion through coordinated actions on apical and basolateral transporters. Whether mineralocorticoids act through H(+),K(+)-ATPases to maintain K(+) and acid-base homeostasis is unknown. Here, treatment of mice with the mineralocorticoid desoxycorticosterone pivalate (DOCP) resulted in weight gain, a decrease in blood [K(+)] and [Cl(-)], and an increase in blood [Na(+)] and [HCO(3)(-)]. DOCP treatment increased the rate of H(+),K(+)-ATPase-mediated H(+) secretion in intercalated cells of the inner cortical collecting duct. mRNA expression of the catalytic subunit HKalpha(1) did not significantly change, whereas HKalpha(2) mRNA expression dramatically increased in the outer and inner medulla of DOCP-treated mice. A high-K(+) diet abrogated this increase in renal HKalpha(2) expression, showing that DOCP-mediated stimulation of HKalpha(2) expression depends on dietary K(+) intake. DOCP treatment of mice lacking HKalpha(1) (HKalpha(1)(-/-)) resulted in greater urinary Na(+) retention than observed in either wild-type mice or mice lacking both HKalpha(1) and HKalpha(2) (HKalpha(1,2)(-/-)). DOCP-treated HKalpha(1,2)(-/-) mice exhibited a lower blood [HCO(3)(-)] and less Na(+) and K(+) retention than either wild-type or HKalpha(1)(-/-) mice. Taken together, these results indicate that H(+),K(+)-ATPases-especially the HKalpha(2)-containing H(+),K(+)-ATPases-play an important role in the effects of mineralocorticoids on K(+), acid-base, and Na(+) balance. |
