Excitatory amino acids in the rostral ventrolateral medulla support blood pressure in spontaneously hypertensive rats

Injection of the excitatory amino acid (EAA) antagonist kynurenic acid (KYN ) into the rostral ventrolateral medulla (RVLM) of anesthetized rats has no effect on arterial pressure. However, we recently reported that after inhi bition of the caudal ventrolateral medulla, injection of KYN into the RVLM decreased arterial pressure to the same level as produced by complete inhib ition of the RVLM. We have suggested that these results reflect tonically a ctive EAA-mediated inputs to the RVLM producing both direct excitation of R VLM vasomotor neurons and indirect inhibition of these neurons. On the basi s of this model, we hypothesize that the balance between these EAA-driven d irect excitatory and indirect inhibitory influences on the RVLM may be alte red in models of experimental hypertension. To begin to test this hypothesi s, the effects of injecting KYN into the RVLM of spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) were compared. In chloralose-anesth etized WKY, bilateral injection of KYN into the RVLM did not alter arterial pressure, whereas similar injections in SHR reduced mean arterial pressure by approximate to 40 mm Hg. After inhibition of the caudal ventrolateral m edulla, which similarly increased arterial pressure in both strains, inject ion of KYN into the RVLM reduced mean arterial pressure to the same level a s produced by autonomic blockade. These results suggest that the balance of excitatory and inhibitory influences on RVLM vasomotor neurons driven by t onically active EAA-mediated inputs to the RVLM is disrupted in SHR and may contribute to the hypertension in SHR.