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the @thebyrdlab asks for a brief explanation of the potassium switch. What follows is a view of our Research Network, @HibpK
1/The Renal potassium switch provides one mechanism to explain the mysterious effects of potassium on BP. Its existence was first suggested when mutations in WNK kinases were identified as a cause of a genetic intolerance to Na+ and K+ (Gordon syndrome, Familial HyperkalemicHTN.
2/Since then, it has become evident that WNK kinases orchestrate a switch response that toggles the activities of two distal nephron segments (Distal Convoluted Tubule, DCT; and Aldosterone Sensitive Distal Nephron, ASDN) to maintain Na+ and K+ balance over widely varied K+ diet
4/Low potassium turns on the switch in the DCT, and this activates the thiazide-sensitive sodium chloride co-transporter (NCC), causing sodium retention. By limiting sodium delivery to the ASDN, potassium excretion is reduced.
5/The switch pathway is ideally adapted for the feast and famine diets of ancient times when dietary salt consumption was low, but it is ill-suited for the current “Westernized diet”. The switch prioritizes K+ retention over sodium excretion.
6/As low K+ consumption, common in modern diets, presses the switch pathway to conserve K+ at the expense of increasing sodium, it feeds the fire of salt-sensitive hypertension and the associated cardiovascular complications.
