Some studies in experimental renal hypertension.
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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.
Female rats were fed diets containing either excess sea salt or excess sodium chloride for periods up to 14 months. The hypertension produced by sea salt was more pronounced than that caused by sodium chloride alone, although the average amount of sodium chloride contained in the sea salt feeding was slightly less. The ions involved in this incremental effect of sea salt were not identified.
Hypertension was induced in female rats by chronic feeding of sodium-containing salts in excess. The hypertension so induced appeared to be self-sustaining since about two-thirds of the animals failed to show a significant fall in blood pressure after withdrawal of these salts from the diet. Under the conditions of these experiments a lack of response to restriction of dietary sodium does not exclude an etiologic relationship between salt intake and development of hypertension.
1. Marked hypertension was induced in adrenalectomized rats on a sodium-restricted intake by the administration of cortisone acetate; on a similar regimen, adrenalectomized rats receiving DCA failed to become hypertensive. 2. The incorporation of a liberal amount of sodium in the diet of adrenalectomized rats receiving cortisone acetate resulted in a lesser degree of hypertension; whereas on a similar regimen, DCA-injected animals became strikingly hypertensive, as has been previously reported. 3. The presence of hypertension in the cortisone acetate-treated rats was not associated with histological evidence of renal damage or serum electrolyte disturbance, such as was observed in hypertensive animals receiving DCA. 4. The hypertension in sodium-restricted normal rats receiving cortisone acetate was less striking than in similarly treated adrenalectomized animals. On a liberal sodium intake similar degrees of hypertension were noted in both intact and adrenalectomized groups. 5. To approximate the loss of weight which occurred in cortisone acetate-injected rats, it was necessary to curtail the food intake of partially fasted control groups to 50 to 75 per cent of the amount consumed by the animals receiving the steroid. 6. The serum cholesterol levels of the cortisone acetate-injected rats were consistently and strikingly elevated as contrasted with normal, partially fasted, or DCA-treated animals.
Sustained arterial hypertension developed in male, albino rats chronically fed diets rich in sodium chloride with demineralized drinking water available ad libitum. After 12 months of the experimental regimen a positive, linear correlation (r = 0.91) was found between the systolic blood pressure and the concentration of sodium chloride in the diet. A syndrome of edema and renal failure was observed in 18 per cent of the group fed at the level of 7.0 to 9.8 per cent of sodium chloride. Significant histologic changes occurred in the kidneys and certain other organs in rats consuming rations containing these levels of NaCl. The relative volume of the radiosodium space was increased in the rat by high dietary sodium chloride.
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