T H E Reaction of Peripheral Blood Vessels to Angiotonin, Renin, and Other Pressor Agents* by Richard

One of the characteristics of the pressor substance which may cause essential hypertension in man or experimental renal hypertension in dogs must be an ability to elevate arterial pressure by constricting the arterioles sufficiently to increase peripheral resistance but not sufficiently to reduce blood flow. Clinical experience indicates that patients or animals with hypertension do not have cold, pale skin indicative of reduced blood supply. On the contrary, the plethoric appearance of many such patients is well known. Experiments, both on animals and man, show that the ability of pressor substances to cause vasoconstriction varies greatly, not only in the same, but in different segments of the vascular system. For example, pitressin and adrenalin have in common the ability to reduce blood flow severely while the former elevates arterial pressure but little and the latter strongly. As Landis, Montgomery, and Sparkman (1) pointed out, pressor agents which severely reduce blood flow to the periphery in relation to their ability to raise blood pressure, could scarcely be expected to be concerned in the genesis of hypertension characterized by normal or even elevated peripheral blood flow. They found in rabbits that renin was unusual among the other pressor substances in elevating arterial pressure without consistent reduction of skin temperature, --which was accepted as a rough measure of peripheral blood flow. The demonstration that renin itself was not a pressor substance but produced elevation of pressure only after interaction with renin-activator and the liberation of angiotonin (2, 3) required that it also be shown that purified angiotonin elevates arterial pressure without significant fall in peripheral blood flow. Corcoran and Page (4) found no consistent change in skin temperature of trained normal dogs when angiotonin was infused. Both renin and angiotonin