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Further evidence has been obtained that L-norepinephrine infusions markedly decreases cutaneous capillary blood flow in the nailfold. Sustained ischemia of the capillary bed occurred prior to the attainment of hypertensive diastolic arterial blood pressure levels. Corroborative evidence of this nailfold capillary ischemia was obtained from the capillary reactive hyperemia that followed the abrupt discontinuance of the L-norepinephrine infusions. The infusion of angiotonin into persons with normal blood pressure did not induce sustained ischemia of the nailfold capillary vessels, even after definite hypertensive diastolic arterial blood pressure levels were attained. Corroboration of the adequacy of nailfold capillary blood flow was obtained by noting the absence of capillary reactive hyperemia following the abrupt cessation of the angiotonin infusions. The nailfold capillary bed in persons with angiotonin-induced hypertension could not be distinguished from that of persons with essential hypertension by direct microscopic examination. During the infusion of angiotonin into subjects with normal cardiovascular systems, the reactivity of the nailfold capillary bed to circulating L-norepinephrine was significantly increased, approaching the levels found in persons with essential hypertension. From the standpoint of its effects upon the nailfold capillary bed, angiotonin, unlike L-norepinephrine, is one substance which possesses the properties required of the hypothetical humoral pressor substance of essential hypertension.

THE RELATION OF ANGIOTONIN AND L-NOREPINEPHRINE TO ESSENTIAL HYPERTENSION AS DETERMINED BY THE REACTION OF THE NAILFOLD CAPILLARY BED