Recent studies have identified a region in the rostral ventromedial medulla (RVMM) of rats that appears to be involved in cardiovascular function. Since these studies used either microinjection of lidocaine or electrical stimulation, the exact contribution of intrinsic neurons as opposed to fibers of passage could not be determined. The present study was performed to map the location of neurons in RVMM from which changes in mean arterial pressure could be elicited by the microinjection of the excitatory amino acid analogue A'-methyl-D-aspartic acid (NMDA) (20 ng/50 nl), which selectively activates cell bodies in barbiturate-anesthetized rats. Microinjection of NMDA into RVMM most often (53%) elicited pressor responses (31 ±7 mm Hg). On the basis of these responses, RVMM was determined to encompass a large portion of the nucleus gigantocellularis 0.5-1.5 mm lateral to the midline, 0.5-3.5 mm above the ventral surface, and extending from the rostral to the caudal pole of the facial nucleus. Depressor responses (—21±3 mm Hg) were found at all levels of RVMM but were most concentrated and of the largest magnitude in the rostral and caudal poles of RVMM. Microinjection of the inhibitory neurotransmitter glycine (500 mM) was used to determine whether neurons in RVMM were contributing to the maintenance of arterial pressure. Microinjection of glycine decreased arterial pressure ( -15±2 mm Hg) throughout most of RVMM. Unexpectedly, increases in mean arterial pressure (24±3 mm Hg) were elicited by microinjection of glycine into the same region in RVMM in which NMDA most frequently elicited pressor responses. These studies show that 1) RVMM contains neurons capable of influencing vasomotor tone, 2) at least some of these neurons contribute to the maintenance of neurogenic tone in anesthetized rats, and 3) microinjection of glycine into RVMM can increase mean arterial pressure by an as yet undetermined mechanism. (Hypertension 1992;19[suppl H]:H-193-II-197)
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