Analysis of several tissues (kidney, right ventricle, left ventricle, aorta spleen, liver) of dogs with renovascular hypertension revealed significantly less endogenous and tritiated norepinephrine in the soluble cytoplasm of the kidneys and in the right and left ventricle, but a higher specific activity of the tritiated compound in the soluble cytoplasm of the kidney. There was no deficit in the ability of the storage granules to bind norepinephrine. These findings indicate that changes in norepinephrine dynamics play only a secondary role in the pathogenesis of experimental renovascular hypertension.