Propranolol blocks the tachycardia induced by galanin (1-15) but not by galanin (1-29)

Regul Pept. 2002 Jul 15;107(1-3):29-36. doi: 10.1016/s0167-0115(02)00060-5.

Abstract

The efferent pathways involved in the tachycardia induced by intracisternal injections of the N-terminal galanin fragment (1-15) (GAL (1-15)) and galanin (GAL (1-29)) has been evaluated in rats pretreated with the cholinergic antagonist atropine or the beta-antagonist propranolol. The pretreatment with propranolol significantly blocked the tachycardic and vasopressor effect produced by intracisternal injection of GAL (1-15) (p<0.05), but the pretreatment with atropine did not modify these cardiovascular effects. However, the cardiovascular response elicited by GAL (1-29) is modified by the pretreatment with atropine (p<0.05) but not by propranolol. These findings demonstrate that the central cardiovascular action of GAL (1-15), but not GAL (1-29), is mediated by beta-receptor stimulation and this suggests the existence of a different pathway involved in the cardiovascular response produced by the N-terminal galanin fragment as compared with the parent molecule GAL (1-29).

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Atropine / pharmacology
  • Atropine / toxicity
  • Blood Pressure / drug effects
  • Cisterna Magna
  • Galanin / antagonists & inhibitors*
  • Galanin / toxicity
  • Heart Rate / drug effects
  • Male
  • Peptide Fragments / antagonists & inhibitors*
  • Propranolol / pharmacology*
  • Rats
  • Rats, Sprague-Dawley
  • Tachycardia / chemically induced*
  • Tachycardia / drug therapy*
  • Time Factors

Substances

  • Peptide Fragments
  • galanin (1-15)
  • Atropine
  • Galanin
  • Propranolol