Key result
Vasopressin reduces choroid plexus blood flow up to ~70% via V1 receptors, sparing cerebral perfusion.
The goal of this study was to examine humoral mechanisms that regulate blood flow to the choroid plexus. We determined the effects of arginine vasopressin on blood flow (microspheres) to the choroid plexus in anesthetized and awake rabbits. In anesthetized rabbits, blood flow to the choroid plexus was 342 +/- 31 (mean +/- SEM) ml/min/100 g under control conditions. Intravenous infusion of vasopressin at 4 and 40 mU/kg increased plasma vasopressin levels from 11 +/- 1 to 55 +/- 15 and 441 +/- 120 pg/ml, respectively, and blood flow to the choroid plexus decreased by 48 +/- 6% and 70 +/- 4%. Cerebral blood flow was not affected by infusion of vasopressin. Similar responses to infusion of vasopressin were observed in awake rabbits. The V1 antagonist [d(CH2)5Tyr(Me)AVP] (10 micrograms/kg i.v.) had no effect on resting blood flow, but abolished the effect of vasopressin on blood flow to the choroid plexus. Vasoconstrictor responses of the choroid plexus to intravenous infusion of phenylephrine were not attenuated by the V1 antagonist. Thus, circulating vasopressin, at plasma levels that are observed under physiological and pathophysiological conditions, has marked effects on blood flow to the choroid plexus. These effects appear to be mediated through a V1 receptor. We speculate that vasopressin may play an important role in regulation of blood flow to the choroid plexus and perhaps in the regulation of cerebrospinal fluid production.
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Faraci et al. (1988) studied Humoral regulation of choroid plexus blood flow. Arginine vasopressin vs. Control conditions and V1 antagonist [d(CH2)5Tyr(Me)AVP] (10 micrograms/kg i.v.) was evaluated on Blood flow to the choroid plexus (48% and 70% decrease). Intravenous arginine vasopressin (4 and 40 mU/kg) reduced choroid plexus blood flow by 48% and 70% in rabbits via V1 receptors without affecting cerebral blood flow.
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