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

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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.