Unilateral microinjection of L-glutamate (L-Glu, 0.5-5 nmol) into the locus coeruleus (LC) of rats anesthetized with chloralose elicited decreases in blood pressure and heart rate. The maximal depressor response elicited by injection of L-Glu into the LC was approximately 30 mmHg, and the maximal bradycardic response was approximately 35 bpm. Microinjections into the LC of DL-homocysteic acid (1 nmol) and carbachol (1 nmol), agents which (like L-Glu) stimulate neurons within the LC, also produced depressor and bradycardic responses. Vagal blockade with methyl atropine eliminated the bradycardic response, but had no effect on the decrease in arterial pressure elicited by stimulation of neurons within the LC. Destruction of the noradrenergic neurons of the LC by local administration of 6-hydroxydopamine eliminated the cardiovascular responses elicited by injection of L-Glu or carbachol into the LC. These results are in direct contrast to the pressor response elicited by electrical stimulation of the region containing the LC. Destruction of the LC with 6-hydroxydopamine, which totally eliminated the depressor response to L-Glu, slightly potentiated the pressor response elicited by electrical stimulation of this region. Electrical stimulation of the region containing the LC has also been reported to increase plasma vasopressin levels; this response could not be reproduced by by stimulation of the LC by microinjection of L-Glu. These results indicate that stimulation of the noradrenergic neurons of the rat LC decreases arterial pressure and heart rate. Furthermore, these results suggest that the pressor response elicited by electrical stimulation of this region is not due to stimulation of neurons of the LC.