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|Title:||Localization and characterization of angiotensin II receptor binding and angiotensin converting enzyme in the human medulla oblongata.||Austin Authors:||Allen, A M;Chai, Syn Y;Clevers, J;McKinley, M J;Paxinos, G;Mendelsohn, Frederick AO||Affiliation:||Department of Medicine, Austin Hospital, University of Melbourne, Heidelberg, Victoria, Australia||Issue Date:||8-Mar-1988||Publication information:||The Journal of Comparative Neurology; 269(2): 249-64||Abstract:||Angiotensin II receptor and angiotensin converting enzyme distributions in the human medulla oblongata were localised by quantitative in vitro autoradiography. Angiotensin II receptors were labelled with the antagonist analogue 125I-[Sar1, Ile8] AII while angiotensin converting enzyme was labelled with 125I-351A, a derivative of the specific converting enzyme inhibitor, lisinopril. Angiotensin II receptor binding and angiotensin converting enzyme are present in high concentrations in the nucleus of the solitary tract, the dorsal motor nucleus of vagus, the rostral and caudal ventrolateral reticular nucleus, and in a band connecting the dorsal and ventral regions. In the rostral and caudal ventrolateral reticular nucleus, angiotensin II receptors are distributed in a punctate pattern that registers with neuronal cell bodies. The distribution and density of these cell bodies closely resemble those of catecholamine-containing neurones mapped by others. In view of the known interactions of angiotensin II with both central and peripheral catecholamine-containing neurons of laboratory animals, the current anatomical findings suggest similar interactions between these neuroactive compounds in the human central nervous system. The presence of angiotensin II receptors and angiotensin converting enzyme in the nucleus of the solitary tract, dorsal motor nucleus of vagus, and rostral and caudal ventrolateral reticular nucleus demonstrates sites for central angiotensin II to exert its known actions on vasopressin release and autonomic functions including blood pressure control. These data also suggest a possible interaction between angiotensin II and central catecholeminergic systems.||Gov't Doc #:||2833536||URI:||http://ahro.austin.org.au/austinjspui/handle/1/12857||DOI:||10.1002/cne.902690209||URL:||https://pubmed.ncbi.nlm.nih.gov/2833536||Type:||Journal Article||Subjects:||Aged
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