Angiotonin exists in two forms: an inactive form (angiotonin I) and an active form (angiotonin II) that causes contraction of rabbit aorta strips, with conversion mediated by a plasma enzyme.
This foundational study demonstrates that angiotonin exists in two forms, with angiotonin I requiring conversion by a plasma enzyme to the active angiotonin II to induce vascular contraction.
By means of a spirally cut strip of rabbit thoracic aorta, it has been shown that angiotonin exists in two forms. One form, angiotonin II, causes a contraction of the strip. The other, angiotonin I, is inactive. They are equally pressor when injected intravenously in animals. An enzyme in plasma converts the inactive form to the active form. The identical pressor activity can be explained by the excess of the converting enzyme in the plasma of the intact animal which rapidly converts angiotonin I to angiotonin II. Some patients with hypertension have a greater content of the converting enzyme in their plasma than is found in plasma of normotensive subjects. In addition to the converting enzyme, other factors in plasma enhance the ability of angiotonin and catechol amines to induce constriction of the strip of aorta. These factors may sensitize the mechanisms in the muscle which set up the process of contraction.
O. M. Helmer (1957) studied Hypertension. Angiotonin I and II was evaluated on Contraction of rabbit aortic strip and pressor activity. Angiotonin exists in two forms: an inactive form (angiotonin I) and an active form (angiotonin II) that causes contraction of rabbit aorta strips, with conversion mediated by a plasma enzyme.