Electrical stimulation of the A5 region in the rat has been shown to elicit a rise in blood pressure with no change in heart rate25. However, electrical stimulation excites axons of passage as well as cell bodies. To activate A5 cells more selective, we have stimulated them with monosodium-l-glutamate. The l-glutamate was pressure injected from one barrel of a double-barrelled pipette. The other barrel, filled with Agar/KCl, was used for electrical stimulation. In midbrain-hemisected rats, electrical stimulation of the A5 region elicited a pressor response with no change in heart rate, as before. However, 30 nl microinjections of l-glutamate led to a dose-related decrease in blood pressure and heart rate. The threshold for the depressor response was about 10 mM l-glutamate, and a maximal depressor response of 30 mm Hg was elicited at about 500 mM. To determine if either the pressor or depressor response involved catecholamines, these experiments were repeated in midbrain-hemisected animals whose central noradrenergic and dopaminergic axon terminals were destroyed with intraventricular 6-hydroxydopamine. While the pressor response to electrical stimulation was still present in these animals, the bradycardic and depressor responses to l-glutamate injection were abolished. Finally, the bradycardic and depressor responses were markedly reduced in animals that had been sympathectomized with guanethidine. These results suggest that activation of A5 cells leads to a decrease in blood pressure and heart rate brought about mainly through the sympathetic nervous system. © 1982.
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