Abstract
ENaC in renal physiology controls sodium excretion to achieve blood pressure regulation through the renin‐angiotensin‐aldosterone system. Our recent findings suggest an additional aspect to this channel's regulation of sodium and water homeostasis. AVP stimulates ENaC in low aldosterone states, indicating that sodium reabsorbed through this channel may contribute to the hypertonic medulla drawing free water out of the distal nephron to concentrate urine. To test whether the consequences of activating ENaC depends on simultaneous AQP2 activation, we forced mice to hypernatremia by providing them only with 3% NaCl drinking solution. The activity of ENaC was robust in these animals. This surprising result was dependent on AVP, which also was elevated due to an increase in serum tonicity. Benzamil compromised the ability to concentrate urine of both control mice and mice maintained with 3% saline, appearing as a benzamil‐dependent increase in urine output and a decrease in UOsm. Thus, elevated AVP counters hypernatremia by stimulating ENaC activity to facilitate free water reabsorption through AQP2. In this context, activation of ENaC in the distal nephron is protecting POsm by promoting anti‐aquaresis rather than influencing serum [Na+] via anti‐natriuretic effects.
Published Version
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