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Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors

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Angiotensin II inhibits cortical cholinergic function: implications for cognition.

J M Barnes¹, N M Barnes, B Costall

¹Postgraduate Studies in Pharmacology, School of Pharmacy, University of Bradford, England.

Journal of Cardiovascular Pharmacology

|August 1, 1990

Summary

Angiotensin II (AT II) inhibits acetylcholine release in rat and human brain tissue. Blocking AT II receptors or ACE may enhance cognitive function by removing this inhibition.

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Area of Science:

Neuroscience
Pharmacology
Biochemistry

Background:

The renin-angiotensin system plays a role in central nervous system function.
Angiotensin II (AT II) is a key peptide in this system, with known effects on blood pressure and fluid balance.
Its role in modulating neurotransmitter release, particularly acetylcholine, in brain regions relevant to cognition is less understood.

Purpose of the Study:

To investigate the effect of Angiotensin II (AT II) on acetylcholine release in rat and human brain tissue.
To determine if AT II receptor antagonists can block these effects.
To explore the presence and function of the angiotensin system components in human temporal cortex.

Main Methods:

Measurement of potassium-stimulated [3H]acetylcholine ([3H]Ach) release from rat entorhinal cortex and human temporal cortex slices.
Application of varying concentrations of AT II and specific AT II receptor antagonists.
Assay for angiotensin-converting enzyme (ACE) activity and AT II recognition sites in human temporal cortex.

Main Results:

AT II significantly inhibited [3H]Ach release in a concentration-dependent manner in rat tissue and at a single concentration in human tissue.
The inhibitory effects of AT II were antagonized by a specific AT II receptor antagonist in both rat and human tissues.
ACE activity and AT II recognition sites were confirmed in human temporal cortex tissue.

Conclusions:

Angiotensin II acts as an inhibitory modulator of cholinergic neurotransmission in the rat and human brain.
The findings support the hypothesis that ACE inhibitors may enhance cognitive function by reducing AT II formation and its inhibitory effects on acetylcholine release.