Inhibitory influences from arterial baroreceptors on vasopressin release elicited by fastigial stimulation in rats.

Abstract

Electrical stimulation of the fastigial nucleus in anesthetized, paralyzed, and artificially ventilated rats for 10 seconds (50 Hz) induced a stimulus-locked elevation of arterial pressure (the fastigial pressor response) and increased plasma vasopressin. Cervical spinal cord transection abolished the stimulus-locked fastigial pressor response and augmented the vasopressin response to a 10-fold increase (19 +/- 1 to 188 +/- 58 pg/ml, P less than 0.05; n = 8). Grading the pressor elevations occurring during the fastigial nucleus stimulus changed the amounts of vasopressin released in the same animal: acute adrenalectomy and chemosympathectomy by guanethidine reduced the magnitude of the fastigial pressor response and facilitated the vasopressin release to fastigial nucleus stimulation (intact: 52 +/- 11 pg/ml; after adrenalectomy and chemosympathectomy, 254 +/- 73 pg/ml, P less than 0.05, n = 6). Subsequent intravenous administration of a bolus of phenylephrine to increase mean arterial pressure during fastigial nucleus stimulus, as in intact situation, reduced the vasopressin release (47 +/- 9 pg/ml). After sinoaortic denervation plus vagotomy, the fastigial pressor response was preserved; however, vasopressin still increased 11-fold (from 11 +/- 1 to 126 +/- 23 pg/ml, P less than 0.01, n = 8). Vagotomy alone did not affect the vasopressin resting level nor the 4-fold increase in response to fastigial nucleus stimulation. Therefore, stimulus-locked elevations of arterial pressure oppose, by reflex mechanisms mediated through baroreceptors, but do not prevent the release of vasopressin elicited by stimulation of the fastigial nucleus.