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Title: Angiotensin II inhibits cortical cholinergic function: Implications for cognition

Abstract

In the present studies we have shown that angiotensin II (AT II), in a concentration-dependent manner in rat tissue (10(-9)-10(-5) M) or at a single concentration in human tissue (10(-6) M), can inhibit potassium-stimulated release of (3H)acetylcholine ( (3H)Ach) from slices of rat entorhinal cortex and human temporal cortex preloaded with (3H)choline for the biochemical analyses. The inhibitory effects of AT II (10(-6) M) were antagonised by the specific AT II receptor antagonist (1-sarcosine, 8-threonine)AT II in a concentration-dependent manner in rat tissue (10(-11)-10(-8) M) and at the single concentration employed in the human studies (10(-7) M). Also demonstrated were other components of the angiotensin system in the human temporal cortex; ACE activity was present (1.03 nmol min-1 mg-1 protein), as were AT II recognition sites (Bmax = 8.6 fmol mg-1 protein). It is hypothesised that the potential cognitive enhancing properties of ACE inhibitors may reflect their action to prevent the formation of AT II and so remove an inhibitory modulator of cholinergic function.

Authors:
; ; ; ; ; ;  [1]
  1. Univ. of Bradford (England)
Publication Date:
OSTI Identifier:
6374373
Resource Type:
Journal Article
Journal Name:
Journal of Cardiovascular Pharmacology; (USA)
Additional Journal Information:
Journal Volume: 16:2; Journal ID: ISSN 0160-2446
Country of Publication:
United States
Language:
English
Subject:
59 BASIC BIOLOGICAL SCIENCES; ACETYLCHOLINE; SECRETION; ANGIOTENSIN; BIOCHEMICAL REACTION KINETICS; ANIMAL TISSUES; CEREBRAL CORTEX; CHOLINE; DOSE-RESPONSE RELATIONSHIPS; INHIBITION; MAN; RATS; TRACER TECHNIQUES; TRITIUM COMPOUNDS; ALCOHOLS; AMINES; AMMONIUM COMPOUNDS; ANIMALS; AUTONOMIC NERVOUS SYSTEM AGENTS; BODY; BRAIN; CARDIOVASCULAR AGENTS; CENTRAL NERVOUS SYSTEM; CEREBRUM; DRUGS; ESTERS; GLOBULINS; HYDROGEN COMPOUNDS; HYDROXY COMPOUNDS; ISOTOPE APPLICATIONS; KINETICS; LIPOTROPIC FACTORS; MAMMALS; NERVOUS SYSTEM; NEUROREGULATORS; ORGANIC COMPOUNDS; ORGANS; PARASYMPATHOMIMETICS; PRIMATES; PROTEINS; QUATERNARY COMPOUNDS; REACTION KINETICS; RODENTS; TISSUES; VASOCONSTRICTORS; VERTEBRATES; 550201* - Biochemistry- Tracer Techniques

Citation Formats

Barnes, J M, Barnes, N M, Costall, B, Horovitz, Z P, Ironside, J W, Naylor, R J, and Williams, T J. Angiotensin II inhibits cortical cholinergic function: Implications for cognition. United States: N. p., 1990. Web. doi:10.1097/00005344-199008000-00009.
Barnes, J M, Barnes, N M, Costall, B, Horovitz, Z P, Ironside, J W, Naylor, R J, & Williams, T J. Angiotensin II inhibits cortical cholinergic function: Implications for cognition. United States. https://doi.org/10.1097/00005344-199008000-00009
Barnes, J M, Barnes, N M, Costall, B, Horovitz, Z P, Ironside, J W, Naylor, R J, and Williams, T J. 1990. "Angiotensin II inhibits cortical cholinergic function: Implications for cognition". United States. https://doi.org/10.1097/00005344-199008000-00009.
@article{osti_6374373,
title = {Angiotensin II inhibits cortical cholinergic function: Implications for cognition},
author = {Barnes, J M and Barnes, N M and Costall, B and Horovitz, Z P and Ironside, J W and Naylor, R J and Williams, T J},
abstractNote = {In the present studies we have shown that angiotensin II (AT II), in a concentration-dependent manner in rat tissue (10(-9)-10(-5) M) or at a single concentration in human tissue (10(-6) M), can inhibit potassium-stimulated release of (3H)acetylcholine ( (3H)Ach) from slices of rat entorhinal cortex and human temporal cortex preloaded with (3H)choline for the biochemical analyses. The inhibitory effects of AT II (10(-6) M) were antagonised by the specific AT II receptor antagonist (1-sarcosine, 8-threonine)AT II in a concentration-dependent manner in rat tissue (10(-11)-10(-8) M) and at the single concentration employed in the human studies (10(-7) M). Also demonstrated were other components of the angiotensin system in the human temporal cortex; ACE activity was present (1.03 nmol min-1 mg-1 protein), as were AT II recognition sites (Bmax = 8.6 fmol mg-1 protein). It is hypothesised that the potential cognitive enhancing properties of ACE inhibitors may reflect their action to prevent the formation of AT II and so remove an inhibitory modulator of cholinergic function.},
doi = {10.1097/00005344-199008000-00009},
url = {https://www.osti.gov/biblio/6374373}, journal = {Journal of Cardiovascular Pharmacology; (USA)},
issn = {0160-2446},
number = ,
volume = 16:2,
place = {United States},
year = {Wed Aug 01 00:00:00 EDT 1990},
month = {Wed Aug 01 00:00:00 EDT 1990}
}