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 consci ous rats that is caused by a centrally mediated activation of sympathetic d rive and the release of arginine vasopressin (AVP). This study tested the h ypothesis that the tissue surrounding the anteroventral part of the third v entricle (AV3V) plays a role in the expression of the presser responses pro duced by systemically injected EAA analogs. Specifically, we examined wheth er 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 pre sser 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 p resser 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-block ed sham-lesioned rats was abolished by a vasopressin V-1-receptor antagonis t. 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 gang lion-blocked rats (45 +/- 3 vs. 57 +/- 4 mmHg; P < 0.05). This study demons trates that the presser responses to systemically injected EAA analogs are smaller in AV3V-lesioned rats. The EAA analogs may produce presser response s by stimulation of EAA receptors in the AV3V region, or the AV3V region ma y play an important role in the expression of these responses.