STUDIES ON RENAL JUXTAGLOMERULAR CELLS IlL THE EFFECTS OF EXPERIMENTAL RENAL DISEASE AND HYPERTENSION

Following Ruyter's discovery of juxtaglomerular cells (1), Goormaghtigh's investigations led him to implicate these cells in the etiology of hypertension. In renal ischemia, whether in man or experimental animals, he observed hyperplasia and hypergranulation of juxtaglomerular cells. He believed that these changes preceded and might have been responsible for hypertension resulting from renal ischemia (2, 3). Although several independent investigators confirmed Goormaghtigh's observations (4-7), others claimed that juxtaglomerular cells bear no relation to hypertension. However, several facts deserve emphasis: in man, JG 1 granules were found to increase in malignant hypertension with acute uremia but not in essential hypertension without uremia (6, 7) ; in rabbits with cellophane perinephritis, the increase in granules occurred only during the early stages, before the onset of hypertension (5); and in animals in which hypertension had been produced by constriction of only one renal artery, JG granules were not increased in the contralateral kidney (.3, 8) and may actually have become decreased in number (9, 10). Furthermore, we had previously found that temporary changes in blood pressure in intact rats, induced by vasoactive drugs, altered the granulation of juxtaglomerular cells (11), although the changes were of small magnitude. An increase in blood pressure (privine) decreased granulation and a lowering of blood pressure (apresoline) increased granulation of JG cells. From these facts, it was considered important to further elucidate the effect of hypertension per se on JG cells as distinct from renal ischemia. The following experiments were designed for this reason.