Axon destruction and adrenergic systems mediate pressor responses after AV3V lesions.

These studies investigated the neural tissue and peripheral mechanism mediating the transient pressor response following electrolytic ablation of the periventricular tissue surrounding the anteroventral third ventricle (AV3V) of the rat. Arterial blood pressure was monitored in conscious animals for 2 h following either microinjection of kainic acid (AV3V-KA) or electrolytic lesions (AV3V-X) in the AV3V region or control procedures (Cont). Blood pressure did not change in AV3V-KA (4 +/- 3 mmHg) or Cont rats but significantly increased in AV3V-X animals (20 +/- 4 mmHg). The pressor response following AV3V-X was not altered by pretreatment with MK-422 (converting-enzyme inhibitor), TMe-AVP (vasopressin antagonist), or hexamethonium (ganglionic blocker). However, intravenous administration of prazosin (alpha-adrenergic blocker) or bilateral adrenalectomy abolished the increase in blood pressure. Furthermore, plasma concentrations of norepinephrine were significantly higher in AV3V-X rats (1,125 +/- 150 pg/ml) compared with Cont animals (322 +/- 83 pg/ml) following treatment. These data indicate that the acute hypertensive response following AV3V-X is caused by the destruction of fibers of passage and results from circulating catecholamines of adrenal origin.