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

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Abstract
Previous studies have implicated the area postrema (AP) as a site responsible for the centrally mediated neurogenic effects of angiotensin II. To clarify 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 .mu.A, 20-60 Hz); the increases in pressure (average: 30 .+-. 4 mm Hg) were rapid in onset and sustained for the 10- to 20-s 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 [units]). 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 by repeating the same kind of stimuli with electrodes placed in the nucleus tractus solitarii (NTS) which resulted in bradycardia (-41 .+-. 6 beats/min) and hypotension (-29 .+-. 5 mm Hg). The fall in blood pressure during NTS stimulation was secondary to the pronounced bradycardia and decreased cardiac output. AP is apparently part of a previously unrecognized pathway which is distinct from the primary baroreflex pathway with relays in the adjacent NTS.