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:
-
- 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}
}