Abstract
In study of the mechanism of renal hypertension, attention has been concentrated on investigation of the role of neurogenic component. Several reports (1-3) have suggested that there are some relations between action of angiotensin and function of the sympathetic nerve endings. Lewis (3) suggested that the action of angiotensin on the vessel wall may result from local release of catecholamine from the sympathetic nerve endings. McCubbin and Page (2) found that infusion of angiotensin caused marked enhancement of the cardiovascular response to agents and procedures causing the release of endogenous noradrenaline.
The present experiments were undertaken primarily to examine whether the adrenergic mechanism is involved in the process of the vasoconstrictor action of angiotensin. In these experiments isolated rabbit ear vessels were perfused. The second object of the experiments was to test whether release of noradrenaline from sympathetic nerve endings could be augmented during the infusion of angiotensin which causes an elevation of the blood pressure. For this study, urinary catecholamine and their orthomethylated products were measured after the infusion of angiotensin. Tyramine which causes release of noradrenaline from sympathetic nerve endings was used to study the functional state of the sympathetic nerve endings.
