Lesions of the AV3V region attenuate sympathetic activation but not the hypertension elicited by destruction of the nucleus tractus solitarius

Abstract

Previous studies have implicated a functionally defined area of the forebrain, the anteroventral third ventricle (AV3V) region as being involved in the regulation of blood pressure and required for the expression of neurogenic hypertension. The present study re-examined the effect of AV3V lesion on hypertension caused by the destruction of the nucleus tractus solitarius (NTS), focussing on whether ablation of the AV3V region altered either the sympathoadrenal or vasopressin (VP) components of NTS hypertension. Bilateral electrolytic lesions of the NTS elicited acute severe hypertension in conscious, freely moving rats whether or not the animals had received AV3V or Sham lesions 14 days previously. Mean arterial pressure (MAP) measured 45 min following NTS lesion was 157 ± 6 mm Hg in AV3V + NTS lesioned rats and 161 ± 7 mm Hg in SHAM + NTS lesioned rats. Plasma VP levels were similarly elevated in the two groups of NTS lesioned animals, and the contribution of VP to the hypertensive response (as assessed by the decrease in arterial pressure in response to a VP pressor antagonist) was the same in both groups. In contrast, NTS lesion appeared to produce a lesser degree of sympathetic nervous system activation in AV3V lesioned rats, as evidenced by a substantially smaller increase in plasma norepinephrine (NE) levels. These results demonstrate that AV3V lesions do not attenuate or prevent NTS hypertension. However, AV3V lesions do appear to attenuate the sympathoadrenal activation caused by NTS lesions.