Chronische Verschlußkrankheiten der Arterien

These experiments indicate that, in dogs at least, ischemia localized to the kidneys is a sufficient condition for the production of persistently elevated systolic blood pressure. When the constriction of both main renal arteries is made only moderately severe in the beginning, the elevation of systolic blood pressure is unaccompanied by signs of materially decreased renal function. In this respect the hypertension in these animals resembles the hypertension which is associated with so called benign nephrosclerosis in man. Subsequent increase of the constriction of the main renal arteries does not materially damage renal function, probably because of adequate development of accessory circulation. More delicate methods for detecting a change may yet prove that some damage does occur. Almost complete constriction of both main renal arteries, from the beginning, results in great elevation of systolic blood pressure which is accompanied by severe disturbance of renal function and uremia. This resembles the type of hypertension which is associated with so called malignant nephrosclerosis, in the sense of Fahr (17). In several of the animals with persistent elevation of systolic blood pressure, anatomical changes were observed in the glomeruli, vessels and parenchyma of the kidneys which are most probably directly referable to the ischemia. It is hoped that these investigations will afford a means of studying the pathogenesis of hypertension that is associated with renal vascular disease.

1. Renin reacts with renin-activator to form a strong pressor substance which is heat-stable, water- and alcohol-soluble, fluorescent, acid-stable, and alkali-labile. It is a reducing substance and is destroyed by strong oxidizing substances. It forms crystalline salts with oxalic and picric acids. The color reaction for arginine is the only one found to be strongly positive. It is suggested that this substance be called angiotonin. 2. Angiotonin produces a sharp, immediate rise in arterial pressure when injected intravenously. Pithing and dissipation of the anesthetic appear to increase the response. Tachyphylaxis occurs, in contrast to renin, only after many single doses. 3. The responses to adrenaline and angiotonin do not parallel one another. Cocaine, atropine, and stilbestrol do not affect the pressor action of angiotonin. Suprarenalectomy in brief experiments is also without effect. 4. Maximal amounts of angiotonin result when the proportion between renin and activator is roughly 3 to 100. This is not a stoichiometric relationship in the chemical sense. The temperature suitable for good yields is about 38°C., and the time of reaction from 10 to 20 minutes. 5. Renin destroys angiotonin when incubated with it. 6. Angiotonin causes marked contraction of intestinal segments of rabbits without reducing their rhythmic motion. It sensitizes the intestine to further doses of angiotonin and alters the intestine such that renin-activator contracts it. Angiotonin also constricts the vessels of a rabbit's ear perfused with blood or Ringer's solution.