Baroreceptor-vasomotor reflex after N-methyl-D-aspartate receptor blockade in rabbit caudal ventrolateral medulla.

AUTOR(ES)

Blessing, W W

RESUMO

1. Experiments were performed in anaesthetized rabbits to determine whether blockade of N-methyl-D-aspartate receptors in the caudal ventrolateral medulla oblongata prevents the changes in renal sympathetic vasomotor activity which normally occur in response to increases or decreases in arterial pressure. 2. N-Methyl-D-aspartic acid receptor blockade using bilateral injections of either kynurenic acid (5 nmol) or DL-amino-5-phosphonovaleric acid (5 nmol) caused a rise in arterial pressure with a variable change in renal sympathetic nerve activity. 3. The depressor and renal sympathoinhibitory responses normally seen after intramedullary injection of N-methyl-D-aspartic acid (50 pmol) into the caudal ventrolateral medulla were entirely prevented by prior receptor blockade. The corresponding responses to L-glutamate (10 nmol) were not affected. 4. The depressor and renal sympathoinhibitory responses normally seen with electrical stimulation of the aortic depressor nerve were abolished by the receptor blockade. 5. The reflex inhibition of renal sympathetic nerve activity normally seen in response to increasing arterial pressure using a cuff around the descending aorta was not affected by kynurenic acid. The response was reduced by DL-amino-5-phosphonovaleric acid but a significant degree of inhibition was preserved. The reflex increase in renal sympathetic nerve activity normally seen in response to reducing arterial pressure using a cuff occluder around the inferior vena cava was unchanged after injection of DL-amino-5-phosphonovaleric acid and was increased in magnitude after injection of kynurenic acid. 6. The results indicate that blockade of excitatory amino acid receptors in the caudal ventrolateral medulla of the rabbit abolishes the depressor response evoked by electrical stimulation of the aortic nerve but leaves intact the normal baroreceptor-vasomotor responses elicited by raising or lowering arterial pressure.

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