Effect of vasopressin on production of cerebrospinal fluid: Possible role of vasopressin (V1)-receptors

F. M. Faraci, W. G. Mayhan, D. D. Heistad

Research output: Contribution to journalArticle

68 Citations (Scopus)

Abstract

The goal of this study was to examine the role of arginine vasopressin in humoral regulation of choroid plexus function. Production of cerebrospinal fluid (CSF) was measured in anesthetized rabbits with an indicator dilution method, by using ventriculocisternal perfusion of artificial CSF containing blue dextran. Rabbits received either vehicle, vasopressin, or vasopressin in the presence of the V1-antagonist [1-(β-mercapto-β,β-cyclopentamethylene propionic acid), 2-(O-methyl)tyrosine]arginine vasopressin {[d(CH2)5Tyr(Me)]-AVP}. Under control conditions, blood flow to the choroid plexus (measured with microspheres) averaged 369 ± 26 (mean ± SE) ml · min-1 · 100 g-1 and CSF production averaged 9.9 ± 0.9 μl/min. Intravenous infusion of vasopressin (2 mU · kg-1 · min-1 for 90 min) decreased blood flow to the choroid plexus by 50-60% for the entire period of infusion. Vasopressin decreased production of CSF by 35 ± 8%. Blood flow to the choroid plexus and production of CSF did not change signficantly from control values in animals that received vehicle. In the presence of the V1-antagonist (10 μg/kg), infusion of vasopressin had no effect on blood flow to the choroid plexus or production of CSF. Thus circulating vasopressin, at plasma levels that are observed under physiological and pathophysiological conditions, has important effects on formation of CSF, as well as on blood flow to the choroid plexus. These findings are consistent with the hypothesis that effects of vasopressin on both variables are mediated through vasopressin (V1)-receptors.

Original languageEnglish (US)
Pages (from-to)R94-R98
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume258
Issue number1 27-1
StatePublished - Jan 1 1990

Fingerprint

Vasopressin Receptors
Choroid Plexus
Vasopressins
Cerebrospinal Fluid
Arginine Vasopressin
Rabbits
Microspheres
Intravenous Infusions
Tyrosine
Perfusion

Keywords

  • Blood flow
  • Choroid plexus
  • Rabbit
  • V-antagonist

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

Effect of vasopressin on production of cerebrospinal fluid : Possible role of vasopressin (V1)-receptors. / Faraci, F. M.; Mayhan, W. G.; Heistad, D. D.

In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 258, No. 1 27-1, 01.01.1990, p. R94-R98.

Research output: Contribution to journalArticle

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abstract = "The goal of this study was to examine the role of arginine vasopressin in humoral regulation of choroid plexus function. Production of cerebrospinal fluid (CSF) was measured in anesthetized rabbits with an indicator dilution method, by using ventriculocisternal perfusion of artificial CSF containing blue dextran. Rabbits received either vehicle, vasopressin, or vasopressin in the presence of the V1-antagonist [1-(β-mercapto-β,β-cyclopentamethylene propionic acid), 2-(O-methyl)tyrosine]arginine vasopressin {[d(CH2)5Tyr(Me)]-AVP}. Under control conditions, blood flow to the choroid plexus (measured with microspheres) averaged 369 ± 26 (mean ± SE) ml · min-1 · 100 g-1 and CSF production averaged 9.9 ± 0.9 μl/min. Intravenous infusion of vasopressin (2 mU · kg-1 · min-1 for 90 min) decreased blood flow to the choroid plexus by 50-60{\%} for the entire period of infusion. Vasopressin decreased production of CSF by 35 ± 8{\%}. Blood flow to the choroid plexus and production of CSF did not change signficantly from control values in animals that received vehicle. In the presence of the V1-antagonist (10 μg/kg), infusion of vasopressin had no effect on blood flow to the choroid plexus or production of CSF. Thus circulating vasopressin, at plasma levels that are observed under physiological and pathophysiological conditions, has important effects on formation of CSF, as well as on blood flow to the choroid plexus. These findings are consistent with the hypothesis that effects of vasopressin on both variables are mediated through vasopressin (V1)-receptors.",
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