High Blood Pressure, also called hypertension, is the largest contributor of premature death and disability in the world. Unfortunately, the basis of hypertension is unknown, and current treatment strategies are suboptimal. High dietary salt (NaCl) consumption has long been considered to be the primary culprit, but growing evidence indicates that low dietary potassium plays an equally important role. Our network unites leaders in the field to rapidly accelerate understanding of a new pathway that may explain the mysterious interaction between dietary potassium, salt-retention and blood pressure.
The Potassium Switch
The “Potassium switch” concept was born out of the discovery of a genetic intolerance to sodium and potassium in humans, caused by mutations in the With-No-Lysine(K) kinases (WNK). Subsequent studies of our group and others revealed that WNK kinases orchestrate a switch response that toggles the activities of sodium and potassium transporters in the kidney to maintain sodium and potassium balance over widely varied potassium intake. Because low potassium consumption, common in modern diets, presses the pathway to conserve potassium at the expense of increasing sodium absorption, the switch provides a mechanism to explain how the modern diet feeds the fire of salt-sensitive hypertension. Our network unites leaders in the field with skills in gene editing, physiology, systems biology, molecular anatomy, and clinical-translational studies to rapidly accelerate understanding of this new pathway and identify new drug targets.