Arch Surg. 1940;41(6):1394-1413. doi:10.1001/archsurg.1940.01210060091009.
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The recent contributions of Goldblatt and his associates1 have placed renal ischemia as a cause of hypertension in the center of interest. When the ischemic tissue was removed or when circulation was reestablished, the experimental hypertension disappeared. Goldblatt2 made the significant observation that "if before constricting the renal artery the kidney is decapsulated and adipose or muscle tissue is attached to the denuded cortical surfaces, the accessory circulation from the adherent tissues becomes very prominent and interferes with the development of pronounced elevation of blood pressure." Animals survive complete closure of both main arteries "when effected gradually by increasing the constriction at intervals. This is proof that such accessory circulation can be functionally highly effective." Verney and Vogt3 have observed that collateral circulation through the capsule or the hilus of the kidney may be sufficient to restore the increased blood pressure to normal in an animal with


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