Cardiovascular Effects of Angiotensin Mediated by the Central Nervous System

During recent years the nature of the considerable contribution of the sympathetic nervous system to renal hypertension has become somewhat more clear, due in part to the unexpected discoveries that angiotensin is not simply a direct vasoconstrictor agent but is almost ubiquitous in its actions.Among these actions are several on the sympathetic nervous system that appear to intensify its effects on the peripheral vascular system.It stimulates release of catechols from the adrenal medulla (1); at certain dose levels it facilitates ganglionic transmission (2); and it sensitizes the neurovascular effector so that the effects of sympathetic vasomotor discharge are augmented (3).This latter effect may depend in part on prevention of reuptake of released norepinephrine (4).For a long time it was considered unlikely that angiotensin had any effect on the central nervous system since theoretically it does not cross the blood-brain barrier.Then Bickerton and Buckley (5), in 1961, cross-perfused the head of a recipient dog, isolated from its own circulation and connected to the body only by the spinal cord, with blood from a donor animal.When angiotensin was injected into the circulation of the donor animal it raised the systemic arterial pressure in the recipient's trunk as well as in the donor animal.Because