Considerable impetus was given to the study of hypertension when Goldblatt1 showed that persistent hypertension could be produced experimentally in dogs by partial clamping of the renal artery. The years that followed brought an extensive literature, based on a renal origin of hypertension. Page2 showed that persistent hypertension could also be induced by enclosing the kidney in a sac of cellophane, which produced a constricting capsule of scar tissue. The "ischemic" kidney was shown to contain increased amounts of a substance, renin,3 which combined in the circulation with a renin activator to produce angiotonin, a pressor substance.4 Then it was found that normal kidney tissue contained an antipressor substance that inactivated angiotonin; this was used by Page and associates5 to treat hypertensive patients and experimental animals. Thus, various humoral factors and antifactors have come to light.
A different point of view was presented when Heymans
GANS JA. CLASSIFICATION OF THE ARTERIOSCLEROTIC-HYPERTENSIVE FUNDUS OCULI IN PATIENTS TREATED WITH SYMPATHECTOMY. Arch Ophthalmol. 1944;32(4):267–275. doi:10.1001/archopht.1944.00890100025002