Effect of potassium depletion on proximal tubule AT1 receptor localization in normal and remnant rat kidney.

Abstract

Since both potassium depletion and renal ablation result in proximal tubule hypertrophy and the angiotensin II type 1 (AT1) receptor has been localized in rat proximal tubules, we explored the possibility that the AT1 receptor intracellular distribution is modulated by potassium depletion in proximal tubular cells of 5/6 nephrectomized (Nx) rats. Four groups of rats were studied: sham operated, potassium-depleted sham-operated rats, 5/6 Nx rats two weeks postsurgery, and potassium-depleted 5/6 Nx rats two weeks postsurgery. After the morphometry of proximal tubular cells was defined, by using immmunogold electron microscopy techniques the subcellular distribution of AT1 receptors were visualized and quantitated. Hypertrophy of proximal tubule cells due to both 5/6 Nx and potassium depletion was documented. Furthermore, to our knowledge for the first time, the results showed that in potassium depletion, with and without superimposed 5/6 Nx, the AT1 receptor density in proximal tubular cells was dramatically enhanced in the apical membrane, the basal membrane, and in nuclei. In normal rats and those subjected to renal ablation, these immunocytochemical data provide intracellular proximal tubule AT1 receptor localization and demonstrate loci of increased receptor density after potassium depletion.