Chronic arterial hypertension has long been recognized as one of the earliest and most important signs of chronic interstitial nephritis, and, together with hypertrophy of the heart and arteriosclerosis, forms a characteristic triad of signs. The several hypotheses which have been advanced to explain these circulatory changes may be classed as either mechanical or chemical.
The purely mechanical explanation, first advanced by Traube, and elaborated into its present widely accepted form by Cohnheim, assumes that the increased blood pressure is an attempt on the part of the heart and arteries to maintain a normal flow of blood through kidneys whose capillary bed has been narrowed to a greater or less degree by the interstitial cirrhosis. The cirrhotic kidney, according to this hypothesis, forms an obstacle to the normal flow of blood, a partial barrier which can be overcome only by a more powerful circulatory pressure. This very plausible explanation which
THE CIRCULATORY CHANGES IN CHRONIC NEPHRITIS. JAMA. 1910;LIV(12):972–973. doi:10.1001/jama.1910.02550380052004
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