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Central adrenergic mechanisms in hemorrhage-induced vasopressin secretion.

Abstract
The effect of central administration of specific adrenergic agonists and antagonists on hemorrhage-induced vasopressin secretion was studied in conscious rats. The intracerebroventricular (icv) injection of the alpha 2-antagonist yohimbine, the alpha 1-antagonist corynanthine, or the beta-agonist isoproterenol failed to alter the vasopressin or blood pressure responses to two sequential 10% reductions in blood volume. Administration of the beta-antagonist propranolol, however, resulted in a significant attenuation of the vasopressin response to hemorrhage, with little effect on the blood pressure response. The alpha 2-agonist, butylated hydroxytoluene (BHT) 933, caused an enhanced vasopressin response to hemorrhage, with a resulting improved maintenance in blood pressure. The results indicate that both alpha 2- and beta-adrenoreceptors may be involved in the pressure-volume control of vasopressin secretion.
AuthorsD P Brooks, L Share, J T Crofton
JournalThe American journal of physiology (Am J Physiol) Vol. 251 Issue 6 Pt 2 Pg. H1158-62 (Dec 1986) ISSN: 0002-9513 [Print] United States
PMID3789169 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)
Chemical References
  • Arginine Vasopressin
  • Butylated Hydroxytoluene
  • Yohimbine
  • Propranolol
  • Isoproterenol
Topics
  • Animals
  • Arginine Vasopressin (metabolism)
  • Blood Pressure (drug effects)
  • Butylated Hydroxytoluene (pharmacology)
  • Hemorrhage (physiopathology)
  • Isoproterenol (pharmacology)
  • Kinetics
  • Male
  • Propranolol (pharmacology)
  • Rats
  • Rats, Inbred Strains
  • Yohimbine (pharmacology)

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