Potassium Homeostasis

Blood pressure regulation is not dependent on sodium intake alone, rather, the ratio of sodium to potassium intake influences blood pressure through changing transporter activity along the nephron.

Even independent of sodium intake, potassium regulation poses challenging questions. In order to maintain an osmotic gradient to drive transport across cell membranes, the body maintains a low extracellular concentration of potassium. This is done even in the face of large intakes (during a meal) and long periods of no intake (between meals) through both feedback and feedforward effects.

We use a computational model of potassium regulation to test our understanding of these regulatory mechanisms during normal conditions and those that induce and treat hyperkalemia. We plan to couple this potassium homeostasis model to our model of blood pressure regulation to explore how the potassium to sodium intake ratio can change blood pressure as well as mechanisms whereby RAS inhibitors can contribute to hyperkalemia.