High Arterial Pressure as a Primary Cause of Hypertensive Vascular Lesions*

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GULL and Sutton1 in 1872 defined the concept of the primacy of “arterio-capillary fibrosis” as the cause of hypertension in the “forbid state called chronic Bright's disease with contracted kidney.” They based their conclusions primarily on studies at necropsy. Mahomed,2 in 1879, reported the opposite conclusion. He was primarily a clinician, and was one of the first to measure arterial pressure and to correlate it with clinicopathologic changes. He3 considered that there were “three stages of chronic Bright's disease: first, the functional stage, which is limited to the condition of high arterial pressure without organic changes in either the vascular system or the kidneys; second, the chronic Bright's disease without nephritis, the stage of organic changes in the vascular system and in the kidney (for which, if thought desirable, the term ‘arterio-capillary fibrosis’ might be employed); third, chronic Bright's disease with nephritis, the natural, but by no means the invariable, termination of the disease.” Unfortunately, Mahomed died while still a young man, and was thus prevented from convincing the medical public by further demonstrations of the natural history of the disease; the authority of the older, presumably wiser, men prevailed.

The demonstration by Goldblatt, Lynch, Hanzal, and Summerville,4 in 1934, that in dogs, partial occlusion of the main renal artery could cause hypertension of varying severity, seemed to support the view that primary nephrosclerosis, if not diffuse “arterio-capillary fibrosis,” might be the true event in hypertension. This concept received further support in 1937 from the observations of Moritz and Oldt5 . . .



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