Experiments to determine whether depressor neurons in the caudal ventrolateral medulla form an integral part of the central pathway transmitting the baroreceptor-vasomotor reflex were performed on rabbits anesthetized with urethan. The function of the depressor neurons was altered by intramedullary injections of agents that stimulate or block receptors for γ-aminobutyric acid and by electrolytic lesions in the caudal ventrolateral medulla. Muscimol abolished both the depressor response and the inhibition of renal nerve activity normally observed after stimulation of the aortic depressor nerve and caused a paradoxical reversal of the depressor response. However, muscimol only partially impaired the inhibition of renal nerve activity produced by experimental elevation of arterial pressure, and it did not affect the increase in renal nerve activity normally produced by decreasing arterial pressure. Bicuculline methiodide amplified the depressor response and the inhibition of renal nerve activity and also restored baroreceptor-vasomotor reflexes abolished by muscimol. Bilateral electrolytic lesions did not alter any component of the baroreceptor-vasomotor reflex. Results indicate that the depressor neurons in the caudal ventrolateral medulla do not form an integral part of the central pathway mediating the baroreceptor-vasomotor reflex. However, output from the depressor neurons appears to inhibit sympathoexcitatory neurons, which also receive baroreceptor-derived inhibitory inputs.
|Number of pages||10|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|Publication status||Published - 1987|