JUXTAGLOMERULAR CELLS AS THE SOURCE OF RENIN: FURTHER STUDIES WITH THE FLUORESCENT ANTIBODY TECHNIQUE AND THE EFFECT OF PASSIVE TRANSFER OF ANTIRENIN.
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Biomedical subjects
Publications and source records attributed to P M HARTROFT.
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Hypertension in rats produced by constriction of one renal artery was associated with degranulation of juxtaglomerular cells in the contralateral, undamped, kidney. These findings are consistent with those of other investigators. Furthermore, the degree of granulation (JGI) in the unclamped kidney was inversely correlated with the level of blood pressure (r = -0.7). Degranulation of JG cells also occurred in rats made hypertensive by application of a "figure-of-eight" ligature to one kidney and removal of the other one, except when the interference in blood supply was so severe that scarring resulted. In these damaged areas, granules persisted or increased in number even though they were decreased in adjacent relatively normal areas. Occlusion of one ureter in rats produced severe hydronephrosis in the homolateral kidney and an elevation in blood pressure. Juxtaglomerular cell granules persisted in the hydronephrotic kidney but were decreased in the contralateral one. This finding confirmed the results of the above experiments. Unilateral nephrectomy in comparable rats had no effect on the degree of granulation of JG cells in the remaining kidney or on the level of blood pressure under the conditions of these experiments. The possibility that degranulation of JG cells in the contralateral kidney in the rats described above was due to compensatory hypertrophy was thereby excluded. An elevation in blood pressure was therefore implicated as an important factor in causing degranulation of juxtaglomerular cells.
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Many of the observations made by Deane and associates (8, 13, 14) regarding the effects of salt restriction, excess salt intake, and hypophysectomy on the zonna glomerulosa of the adrenal cortex in the rat have been confirmed. A positive correlation (r = 0.63) of high statistical significance has been demonstrated between the degree of granulation of JG cells (JGI) and the width of the zona glomerulosa in 159 rats from 5 series of experiments in which low, normal, and high salt regimens were employed. A somewhat higher correlation (r = 0.81) was obtained when only rats were included from the most recent experiment of the series in which JGI counts were more accurate. Under the conditions of these experiments, therefore, increased granulation and degranulation of JG cells were associated with hyperactivity and suppressed activity, respectively, of the zona glomerulosa. Rats sacrificed 4 to 7 weeks after hypophysectomy were found to have normal JG cells. This finding constitutes another example of the similarity in response of JG cells to that of the zona glomerulosa, which also remained unaltered following hypophysectomy despite atrophy of the rest of the adrenal cortex.
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Accumulation of granules in the juxtaglomerular cells occurred in rats which were maintained for 5 to 6 weeks on a diet low in sodium, chloride. Cytological evidence suggests that this was probably a storage phase of secretion following a decrease in the rate of liberation of the granules. Administration of DCA (desoxycorticosterone acetate) to salt-deficient rats did not alter this appearance of the juxtaglomerular cells. Two per cent sodium chloride taken in the drinking water consumed for 4 weeks by similar animals caused degranulation of the juxtaglomerular cells. This effect was enhanced by DCA. DCA administered to animals on a normal salt intake produced a lesser degree of degranulation. Cytological changes in degranulated cells suggested that these represent a stage of hyperactivity in the secretory cycle produced by an increase in the rate of liberation of granules. A hypothesis is suggested that the juxtaglomerular cells are involved in the hormonal regulation of sodium metabolism and/or blood pressure.
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