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.
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