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Modulation of the epithelial Na +  channel (ENaC) activity in the collecting duct (CD) is an important mechanism for normal Na +  homeostasis. ENaC activity is inversely related to dietary Na +  intake, in part due to inhibitory paracrine purinergic regulation. Evidence suggests that H + ,K + -ATPase activity in the CD also influences Na +  excretion. We hypothesized that renal H + ,K + -ATPases affect Na +  reabsorption by the CD by modulating ENaC activity. ENaC activity in HKα 1  H + ,K + -ATPase knockout (HKα 1  −/− ) mice was uncoupled from Na +  intake. ENaC activity on a high-Na +  diet was greater in the HKα 1  −/−  mice than in WT mice. Moreover, dietary Na +  content did not modulate ENaC activity in the HKα 1  −/−  mice as it did in WT mice. Purinergic regulation of ENaC was abnormal in HKα 1  −/−  mice. In contrast to WT mice, where urinary [ATP] was proportional to dietary Na +  intake, urinary [ATP] did not increase in response to a high-Na +  diet in the HKα 1  −/−  mice and was significantly lower than in the WT mice. HKα 1  −/−  mice fed a high-Na +  diet had greater Na +  retention than WT mice and had an impaired dipsogenic response. These results suggest an important role for the HKα 1  subunit in the regulation of purinergic signaling in the CD. They are also consistent with HKα 1 -containing H + ,K + -ATPases as important components for the proper regulation of Na +  balance and the dipsogenic response to a high-salt diet. Such observations suggest a previously unrecognized element in Na +  regulation in the CD.

american journal of physiology. renal physiology./american journal of physiology. renal physiology

ENaC activity in the cortical collecting duct of HKα1 H+,K+-ATPase knockout mice is uncoupled from Na+ intake