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Hyperaldosteronism and Hypergranularity of the Juxtaglomerular Cells in Renal Hypertension: Metabolic Studies

Ann Intern Med. 1963;59(1_Part_1):24-36. doi:10.7326/0003-4819-59-1-24
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In the past few years a series of important investigations has indicated that the kidney plays a key role in the regulatory mechanisms controlling the secretion of aldosterone by the adrenal gland (1-6). Procedures that reduce blood flow or perfusion pressure to the kidney, such as hemorrhage (2, 7), renal artery (4) or suprarenal aortic constriction (6), and sodium depletion (3) cause an increased secretion of aldosterone. The aldosterone hypersecretion in response to hemorrhage and sodium depletion can be prevented by bilateral nephrectomy (2, 3). It has also been demonstrated in animals that the granularity of the juxtaglomerular (JG) cells


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