 In the laboratory of Molecular Biology at the Department of Nephrology P, Rigshospitalet, we have found some interesting results regarding potassium and aldosterone. Working with an in vitro model of aldosterone secretion in the form of the human adrenocortical cell line H295R, which has been proven to be a model for studying the function of the human adrenal cortex 13;14, we found interactions between extracellular potassium and components of the renin-angiotensin-aldosterone system RAAS. The H295R cell line is a model of the human adrenocortical zona glomerulosa cells, which normally are the site of synthesis and secretion of aldosterone in the human body. Aldosterone secretion from these cells is mainly stimulated by angiotensin II Ang II, as part of the activation of the RAAS, and by extracellular potassium in situations with rising levels of extracellular potassium. These two secretagogues are traditionally being look upon as independent. But our studies showed interactions between the two systems. It was found that stimulation of the H295R cells with high levels of extracellular potassium decreased the amount of Ang II type 1 receptors in the membrane of the cells, measured as a fall in the specific binding of radioactive labelled Ang II to the cells 15. This reduction in specific binding of radioactive labelled Ang II, was followed by a potassium induced reduction in the expression of the Ang II type 1 receptor gene AGTR1 15. This means that the Ang II sensitivity of human aldosterone producing cells is reduced by high levels of extracellular potassium in vitro and the hypothesis is that high levels of extracellular potassium thus modulate the renin-angiotensin-aldosterone system. 