Parabrachial nucleus modulation of vasopressin release

The present studies examine the contribution of the ventrolateral lateral parabrachial nucleus (VLLPBN) to the regulation of plasma arginine vasopressin (P(AVP)) release in response to either a baroreceptor or osmotic stimulus. These studies were carried out in rats with bilateral electrolytic lesions of the VLLPBN. Baroreceptor-induced stimulation of P(AVP) was achieved by decreasing blood pressure with combined blockade of the renin-angiotensin system with captopril (3 mg/kg iv) and the sympathetic nervous system with chlorisondamine, (11 mg/kg sc). Osmotic release of vasopressin was elicited by a 2-h intravenous infusion of hypertonic saline, (3.0 meq/ml, 0.01 ml/min). Blood pressure and heart rate were monitored throughout the experiments. Blood samples for determination of P(AVP), plasma osmolality P(osm), plasma sodium (P(Na)), and plasma potassium (P(K)) were taken before (base line) and after treatment in each study. The VLLPBN-lesioned rats secreted significantly more vasopressin in response to hypotension produced by combined renin-angiotensin and sympathetic nervous system blockade than did control rats. There was no significant difference between groups in P(osm), P(Na), or P(K), or cardiovascular changes. In contrast, hypertonic saline infusion did not produce any differential changes between groups.