The specificity of angiotensin II receptor binding in rat brain.
125I-angiotensin II (125I-AII) binding was examined in the hypothalamic-thalamic-septal-midbrain (HTSM) region of HLA-Wistar rats in the presence of CNS-active agents. Angiotensin I, II, and III and saralasin competed for 125 I-AII binding, whereas structurally unrelated peptides such as arginine and lysine vasopressin, oxytocin, LHRH, TRH, bradykinin, and substance P did not. In contrast, ACTH and neurotensin exhibited a weak, dose-dependent competition for 125 I-AII binding. The relative potencies of AII, AI, neurotensin and ACTH were 100:1:0.1:0.05, respectively. Neurotensin and ACTH competition was not additive with AII suggesting interaction at shared binding sites. Most importantly, a wide variety of other CNS active agents such as methyldopa, naloxone, catecholamines, clondidine, and reserpine, failed to inhibit 125 I-AII binding, thus further defining the specificity of the CNS AII receptor.
D000324:Adrenocorticotropic Hormone / Q000378:metabolism; D000804:Angiotensin II / Q000378:metabolism*; D000809:Angiotensins / Q000378:metabolism; D000818:Animals; D001667:Binding, Competitive; D001921:Brain / Q000378:metabolism*; D007031:Hypothalamus / Q000378:metabolism; D008636:Mesencephalon / Q000378:metabolism; D009496:Neurotensin / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D011945:Receptors, Angiotensin / Q000378:metabolism*; D011956:Receptors, Cell Surface / Q000378:metabolism*; D012504:Saralasin / Q000378:metabolism; D012688:Septum Pellucidum / Q000378:metabolism; D013788:Thalamus / Q000378:metabolism
D000809:Angiotensins; D011945:Receptors, Angiotensin; D011956:Receptors, Cell Surface; D000804:Angiotensin II; D009496:Neurotensin; D000324:Adrenocorticotropic Hormone; D012504:Saralasin