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Angiotensin II inhibits the release of [3H]acetylcholine from rat entorhinal cortex in vitro

  • J. M. Barnes
  • , N. M. Barnes*
  • , B. Costall
  • , Z. P. Horovitz
  • , R. J. Naylor
  • *Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

Abstract

The effects of angiotensin I and II on basal potassium-induced release of [3H]acetylcholine were investigated in slices of rat entorhinal cortex. Potassium (10-25 mM) produced a concentration-dependent increase in the release of [3H]acetylcholine in the presence of extracellular calcium. Angiotensin II (10-9-10-5 M) (but not angiotensin I) reduced the potassium-induced release of [3H]acetylcholine in a concentration-related manner to 60% of control levels, but did not effect basal tritium release. The effect of angiotensin II was antagonised by [1-sarcosine, 8-threonine] angiotensin II, an angiotensin II receptor antagonist, but not by agents acting on α- and β-adrenoceptors, muscarinic, nicotinic, histamine or 5-hydroxytryptamine receptors nor by the angiotensin converting enzyme (ACE) inhibitor SQ 29852. The results indicate that angiotensin II acting via an angiotensin II receptor can inhibit the release of [3H]acetylcholine in slices of the rat entorhinal cortex. It is hypothesised that the ability of ACE inhibitors to facilitate cognitive processes may be related to a reduced availability of angiotensin II.

Original languageEnglish
Pages (from-to)136-143
Number of pages8
JournalBrain Research
Volume491
Issue number1
DOIs
Publication statusPublished - 3 Jul 1989

Keywords

  • Acetylcholine release
  • Angiotensin converting enzyme inhibitor SQ 29852
  • Angiotensin II
  • Cognition
  • Entorhinal cortex

ASJC Scopus subject areas

  • General Neuroscience
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

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