Potassium regulates angiotensin II-induced aldosterone biosynthesis in acutely nephrectomized rats.

The studies described herein were designed to determine whether serum potassium modulates the aldosterone secretory response to angiotensin II (Ang II) after nephrectomy. We used isolated adrenal glomerulosa cells harvested from rats maintained with either normal (5.2 meq/liter) or high (6.8 meq/liter) serum potassium for 48 h after bilateral nephrectomy for determining Ang II-aldosterone dose-response relationships. Kayexalate, which exchanges sodium for potassium in the gastrointestinal tract, was used to achieve the desired level of serum potassium. Both groups of cells were responsive to low concentrations of Ang II (10-100 pM). Cells from rats with lower serum potassium levels had lower basal and maximum Ang II-stimulated aldosterone and ED50 values. The importance of variables as contributors to differences between the groups were ranked from most to least important by two group discriminant function analysis and revealed: serum potassium greater than maximum Ang II-stimulated aldosterone greater than ED50 greater than basal aldosterone greater than serum sodium. Stepwise multivariate discriminant analysis demonstrated that all variables except the level of serum sodium contributed to the groups being significantly different at P less than 0.05. These studies demonstrate that adrenal glomerulosa cells obtained from nephrectomized rats maintain sensitive secretory responses to Ang II. Additionally, the level of serum potassium of rats before death directly regulates both the sensitivity and magnitude of the aldosterone secretory response to Ang II in vitro.