STUDIES ON EXPERIMENTAL RENAL HYPERTENSION

Abstract

In order to investigate the causative mechanism of renal hypertension and maintaining mechanism of high blood pressure, observations were made on the histological changes in the constricted kidney, the contralateral kidney, and the blood vessels of the whole body from the second day to the fifty-sixth day after the unilateral renal artery constriction of a rat. Furthermore, the author also observed the changes in the kidney and the blood vessels of the whole body after giving synthesized Angiotensin II. By comparison of the histological changes of both experiments, the following results were observed:
1. Fluctuation of blood pressure caused by the unilateral renal artery constriction was observed after the second day; then blood pressure was gradually elevated and it remained at about 150mmHg.
2. Ischemic changes of the renal parenchyma and wedge-shaped necrosis were clearly found at the same time within a week in the constricted kidney. After a week, proliferation of the nuclei, hypertrophy of endothelium and mesangium of the glomeruli, thickening of Bowman's capsules and cell-infiltration and proliferation of connective tissue in the interstitium appeared; changes of the glomeruli and the interstitium showed a tendency, though very slightly, to increase continually. Thickening of the media in renal arterioles was seen from the fourth day, but this did not show a tendency to become obvious continually. The only changes found in blood vessels was thickening of the media, and neither degeneration nor necrosis was seen. As far as the constricted kidney was concerned, at the early stage ischemic changes were strongly present. But, as time went on, sclerotic changes, though comparatively slight, were observed.
3. In continual observation of the histological changes of the contralateral kidney, only very slight thickening of the media in renal blood vessels was seen within a week; but after two weeks, remarkable thickening of the media was found in arterioles and small arteries. At the same time, some changes began to appear in the glomeruli, tubuli, and interstitium, and they gradually became prominent. But necrosis was not observed in the renal parenchyma or arterial walls.
4. J. G. C. granules increased a little in the constricted kidney three days after the renal artery constriction, and continually increased. On the contrary, J. G. C. granules in the contralateral kidney decreased after a week, and this same tendency to decrease was noted even after eight weeks. The higher the degree of granulation in the constricted kidney, the more markedly and the more rapidly the granules in the contralateral kidney decreased.
5. After four days or so, slight thickening of the media in the arterioles was observed in the blood vessels of the viscera, except in the kidney. After two weeks, remarkable thickening of the media was seen not only in the arterioles but also in small arteries. This change gradually became prominent, but it was limited mainly to the media and partly to the intima. Such changes as exudation of fibrin, hyalinous degeneration, and fibrinoid necrosis were not observed at all.
6. Elevation of blood pressure was observed in all the cases by giving the synthesized Angiotensin II, and the rate of elevation was 45.5mmHg in average. Compared with fluctuation of blood pressure caused by unilateral renal constriction, this rate of elevation was somewhat low.
7. Swelling of the glomeruli, proliferation of the nuclei, hypertrophy of the endothelium and the mesangium, thickening of Bowman's capsules, and cell-infiltration and proliferation of the connective tissue in the interstitium were found in the kidney after giving the synthesized Angiotensin II. Remarkable thickening of arterioles and small arteries was also observed in renal blood vessels in all cases. J. G. C. granules disappeared or diminished in 84.2% of the total cases of this experiment. These histological changes were very similar to those seen