Comparison of the hemodynamic changes produced by electrical stimulation of the area postrema and nucleus tractus solitarii in the dog.

Abstract

SUMMARY Previous studies have implicated the area postrema (AP) as a site responsible for the centrally mediated neurogenic effects of angiotensin II. To clarify further its possible role in the central control of blood pressure, stainless steel electrodes were lowered stereotaxically into the AP of morphine-chloralose-anesthetized dogs after surgical exposure of the walls of the 4th ventricle just anterior to the obex. In all experiments, large pressor responses were obtained at a relatively low stimulus strength (range: 20-80 jiA, 20-60 Hz); the increases in pressure (average: 30 ± 4 mm Hg) were rapid in onset and sustained for the 10- to 20-second duration of the stimulus. Hemodynamically, the pressor response during AP stimulation was due to increases in both cardiac output (+211 ± 37 ml/ min) and peripheral resistance (+0.81 ± 0.33 U). An increase in heart rate contributed to the onset but not the plateau of the pressor response. Reconstruction of electrode tracts in all experiments corroborated that these pressor responses originated in the AP. The specificity of these cardiovascular responses was confirmed further by repeating the same kind of stimuli with electrodes placed in the nucleus tractus solitarii (NTS). In contrast to the effects obtained during AP stimulation, bradycardia (-41 ± 6 beats/min) and hypotension (-29 ± 5 mm Hg) were characteristic features. The fall in blood pressure during NTS stimulation was secondary to the pronounced bradycardia and decreased cardiac output. The data suggest that the AP is part of a previously unrecognized pathway which is distinct from the primary baroreflex pathway with relays in the adjacent NTS. Circ Res 45:136-143, 1979 THE MULTIPLICITY of actions of angiotensin II has led several investigators to explore the possibility that this hormone could have an effect within the central nervous system. This idea, first suggested by Bickerton and Buckley in 1961, lay dormant until recent years when Scroop and Lowe (1968) and Ferrario et al. (1970) showed that the infusion of angiotensin into the circulation of the dog's brain raised arterial blood pressure by a mechanism not involving direct vascular smooth muscle constriction. Since previous experiments (Ferrario et al., 1972; Gildenberg et al., 1973; Joy and Lowe, 1970) showed that the pressor effects of angiotensin in the medulla required the integrity of the area