The Relation of Angiotonin and L-Norepinephrine to Essential Hypertension as Determined by the Reaction of the Nailfold Capillary Bed

Abstract

If a humoral pressor substance is responsible for essential hypertension in man, one of its characteristics should be the ability to constrict the arteriolar bed sufficiently to increase total systemic peripheral resistance, but not sufficiently to reduce cutaneous blood flow. Clinical experience indicates that patients with essential hypertension do not have cold, pale skin reflecting diminished blood flow. More objective studies of total systemic peripheral blood flow in persons with essential hypertension have demonstrated no significant reduction from normal levels (1, 2).This hypothetical pressor substance should also be capable of producing generalized systemic arteriolar constriction without inducing significant constriction or decreased blood flow in a cutaneous capillary bed such as the nailfold. Studies of the nailfold capillary bed in persons with essential hypertension have indicated the absence of significant capillary constriction or decreased capillary blood flow (3, 4).Two naturally occurring pressor agents, norepinephrine and angiotonin, when infused intravenously into persons with normal blood pressure, produce changes in the central systemic circulation similar to those found in persons with essential hypertension (5, 6). The hypertensive state associated with the infusion of norepinephrine however differs markedly from essential hypertension when the circulation in a cutaneous capillary bed such as the nailfold is examined. L-Norepinephrine induces a progressive constriction of this capillary bed as the rate of infusion is increased, so that the nailfold capillary bed is rendered ischemic prior to attainment of hypertensive diastolic arterial blood pressure levels (4).The purpose of the present study was to determine the reaction of a cutaneous capillary bed in persons made hypertensive by the infusion of angiotonin and to compare this reaction with that seen in persons with hypertension induced by L-norepinephrine and in persons with essential hypertension. The vascular bed