Distribution of angiotensin IV binding sites (AT4 receptor) in the human forebrain, midbrain and pons as visualised by in vitro receptor autoradiography

Influence of losartan and atenolol on memory function in very elderly hypertensive patients

“…Blockade of AII at the AT1 receptor level by losartan might also result in an increased synthesis of angiotensin IV; this peptide selectively binds to AT4 receptors, whose activation has been demonstrated to participate in memory acquisition and recall, perhaps via modulating neurotransmitters release and/or remodelling cholinergic and glutaminergic pathways in the hippocampus. [49][50][51] Unlike losartan, atenolol treatment did not significantly affect cognitive performance, which is in agreement with some previous observations showing no improvement, but also no deterioration in cognitive function of hypertensive patients treated with beta-blockers. [28][29][30][31][32] The difference between losartan and atenolol in their effects on cognitive function did not depend on their antihypertensive effect, since the BP reduction was similar with the two drugs.…”

“…[46][47][48] The facilitatory effects of angiotensins on memory has been connected mainly with the recently discovered AT4 receptors, which preferentially bind AIV and AII [3][4][5][6][7] and are found in brain areas distinct from those possessing AT1 and AT2 receptors (mainly in the neocortex, hippocampus, dentate gyrus, thalamus and cerebellum). [49][50][51] However, considerable evidence suggests significant, although different, involvement of AT1 and AT2 receptors in cognitive processes. 52,53 In various animal models of learning and memory, inhibitors of the renin-angiotensin system, particularly ACE inhibitors and AII antagonists, have been reported to have potential nootropic effects.…”

Facilitation of Hippocampal Synaptogenesis and Spatial Memory by C-Terminal Truncated Nle1-Angiotensin IV Analogs

“…Of most importance, the acute application of one of these analogs, Nle 1 -AngIV, reverses deficits in dementia models induced by 1) treatment with the cholinergic muscarinic receptor antagonist scopolamine (Pederson et al, 2001), 2) kainic acid injections into the hippocampus (Stubley-Weatherly et al, 1996), 3) perforant path cuts (Wright et al, 1999), and 4) ischemia resulting from transient four-vessel occlusion . Consistent with these behavioral and electrophysiological results, brain binding sites for 125 I-AngIV have been autoradiographically localized in structures known to mediate cognitive processing including the neocortex, hippocampus, and basal nucleus of Meynert (Harding et al, 1992;Chai et al, 2000;Wright and Harding, 2008). It should be noted that the AT 1 angiotensin receptor subtype may also contribute to the cognitive effects of AngIV (De Bundel et al, 2010).…”

Alzheimer's, Angiotensin IV and an Aminopeptidase

“…[8][9][10][11][12] The distribution between species is consistent with high levels of radioligand binding observed in the motor nuclei and in areas associated with cognitive and sensorimotor functions, such as the hippocampus, neocortex and cerebellum. Of particular interest is the occurrence of high affinity binding in areas associated with memory; areas of basal forebrain cholinergic nuclei, including the medial septal complex and the basal nucleus of Meynert, and their terminal fields, such as the hippocampus and neocortex.…”