PONTINE PRESSOR SITES WHICH RELEASE VASOPRESSIN

Electrical stimulation of sites within the parabrachial nucleus (PBN; 0.2 ms pulses at 50 hz for 10 s, 100 .mu.A) of chloralose-anesthetized rats elicited increases in mean arterial pressure (+34 .+-. 2 mm Hg, n = 13). In rats in which the electrode tip was located in the dorsal and lateral portions of the PBN, electrical stimulation also produced a small increase in plasma levels of arginine vasopressin (VP; 6.7 .+-. 0.9 pg/ml before stimulation to 16.5 .+-. 3.9 pg/ml after, n = 7, P < 0.05). No change in VP levels was observed with stimulation of more medial and ventral portions of the PBN. Following blockade of the autonomic nervous system (by i.v. injection of chlorisondamine plus infusion of phenylephrine to prevent hypotension) VP release in response to stimulation of the lateral and dorsal portions of the PBN was greatly enhanced (8.8 .+-. 1.4 pg/ml following ganglionic blockade but before PBN stimulation and 82 .+-. 27 pg/ml following stimulation, P < 0.01) and this increase in VP release was sufficient to increase arterial pressure (+18 .+-. 3 mm Hg, P < 0.01). Electrical stimulation of the locus coeruleus (LC) produced a pressor response of similar magnitude to that produced by PBN stimulation. LC stimulation also increased plasma VP release (5.6 .+-. 0.3 pg/ml before stimulation, 13 .+-. 3 pg/ml following stimulation, and 30 .+-. 8 pg/ml following stimulation of the ganglionic blocked state; n = 5). These studies demonstrate that stimulation of certain regions of the dorsal pons can elicit VP release into the circulation, and suggest a role of the PBN and LC in the central neural control of VP secretion. Furthermore, since these nuclei have been implicated in cardiovascular control, these results suggest that VP may be involved in cardiovascular regulation exerted by these nuclei.