Abstract
Evidence supports that a negative correlation exists between dietary potassium consumption and blood pressure levels in the population. It has also been well documented that increasing dietary potassium consumption, increases urinary sodium excretion. The molecular mechanisms that contribute to this latter phenomenon are under investigation. Recent evidence suggests that the thiazide-sensitive Na+:Cl- cotransporter, NCC, may play a key role in this regard. For instance, in mouse models, variations in blood pressure and natriuresis observed in response to altered potassium intake are significantly blunted in NCC deficient mice. NCC activity indirectly modulates urinary potassium excretion and NCC activity is tightly regulated in response to subtle alterations in plasma potassium concentration that occur in response to dietary potassium consumption changes. The molecular mechanisms that mediate this modulation are complex and their characterization has significantly advanced in recent years. Such mechanisms will be discussed in the presentation. The most recent advances will be highlighted.
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