AV3V lesions attenuate the cardiovascular responses produced by blood-borne excitatory amino acid analogs

Systemic injections of the excitatory amino acid (EAA) analogs, kainic acid (KA) and N-methyl-D-aspartate (NMDA), produce a presser response in conscious rats that is caused by a centrally mediated activation of sympathetic drive and the release of arginine vasopressin (AVP). This study tested the hypothesis that the tissue surrounding the anteroventral part of the third ventricle (AV3V) plays a role in the expression of the presser responses produced by systemically injected EAA analogs. Specifically, we examined whether prior electrolytic ablation of the AV3V region would affect the presser responses to KA and NMDA (1 mg/kg iv) in conscious rats. The KA-induced presser response was smaller in AV3V-lesioned than in sham-lesioned rats (11 +/- 2 vs. 29 +/- 2 mmHg; P < 0.05). After ganglion blockade, KA produced a presser response in sham-lesioned but not AV3V-lesioned rats (+27 +/- 3 vs. +1 +/- 2 mmHg; P < 0.05). The KA-induced presser response in ganglion-blocked sham-lesioned rats was abolished by a vasopressin V-1-receptor antagonist. Similar results were obtained with NMDA. The presser response to AVP (10 ng/kg iv) was slightly smaller in AV3V-lesioned than in sham-lesioned ganglion-blocked rats (45 +/- 3 vs. 57 +/- 4 mmHg; P < 0.05). This study demonstrates that the presser responses to systemically injected EAA analogs are smaller in AV3V-lesioned rats. The EAA analogs may produce presser responses by stimulation of EAA receptors in the AV3V region, or the AV3V region may play an important role in the expression of these responses.