Using male albino rats, I succeeded in the development of a longterm salt-hypertension (duration, 192-272 days). As the previous report, I investigated various clinical observations, particularly such as sodium chloride metabolism.Salt-loading consisted in the substitution of sod. chloride solution (1-1.5-2.0 %) for the drinking water, and in injection of a 2 % sod. chloride sol. into the abdominal cavity or diets high in sod. chloride (0.2-0.3-0.4g. per day). The increase of this loading was gradually performed.In the course of chronic high salt-loading, the blood pressure levels of the rats exceeded over 200 mm of Hg.In some other rats the elevated blood pressure returned gradually to the control values after cessation of the salt loading.The maximum water intake was 77.2 cc. per 100 g. body weight per day.No increase of N. P. N. in blood was observed, however a transient proteinuria was sometimes found.There was no relationship between urinary output of 17-KS and elevation of blood pressure through this experiment.The changes in the administered salt levels are surely reflected to the increase 17-KS output in urine, presumably as a consequence of any type of stress.The excessive retention of sod. was showed by the investigations of sod. content in serum or muscle and sod. chloride metabolism.The relationship between the elevation of blood pressure and the amount of NaCl retention seems to be proportional.

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In this report, I described discussion and summary about the previous papers (I & II). DCA hypertension is very similar to salt hypertension is very similar to salt hypertension in regards to through the intermedium of sod. chloride.Then, in the both experimental hypertension, the elevation of blood pressure was always observed after the retention of sodium.the important differences in sod. chloride metabolism between DCA rats and NaCl-loading rats were showed to be significant in comparison of the mean or the maximum sod. chloride intakes volume.These differences may be dependent upon the salt-retaining properties of DCA, and so DCA hypertension did not need sod. chloride so mach as salt hypertension in rats.The changes of the adrenal cortex were similar in both DCA-and salt-hypertensive rats (particularly, chronic NaCl-loading rats), namely atrophy of zona glomerulosa and sligh hyperfunction of zona fasciculata.The above results suggest the following view, that sodium may be essential for the pathogenesis of hypertension.

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