{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,12]],"date-time":"2026-06-12T04:37:40Z","timestamp":1781239060200,"version":"3.54.1"},"reference-count":127,"publisher":"Wiley","issue":"16","license":[{"start":{"date-parts":[[2023,6,27]],"date-time":"2023-06-27T00:00:00Z","timestamp":1687824000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100008893","name":"University of Iowa","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100008893","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2023,8]]},"abstract":"<jats:sec><jats:title>Abstract<\/jats:title><jats:p>In addition to its renal and cardiovascular functions, angiotensin signalling is thought to be responsible for the increases in salt and water intake caused by hypovolaemia. However, it remains unclear whether these behaviours require angiotensin production in the brain or liver. Here, we use <jats:italic>in situ<\/jats:italic> hybridization to identify tissue\u2010specific expression of the genes required for producing angiotensin peptides, and then use conditional genetic deletion of the angiotensinogen gene (<jats:italic>Agt<\/jats:italic>) to test whether production in the brain or liver is necessary for sodium appetite and thirst. In the mouse brain, we identified expression of <jats:italic>Agt<\/jats:italic> (the precursor for all angiotensin peptides) in a large subset of astrocytes. We also identified <jats:italic>Ren1<\/jats:italic> and <jats:italic>Ace<\/jats:italic> (encoding enzymes required to produce angiotensin II) expression in the choroid plexus, and <jats:italic>Ren1<\/jats:italic> expression in neurons within the nucleus ambiguus compact formation. In the liver, we confirmed that <jats:italic>Agt<\/jats:italic> is widely expressed in hepatocytes. We next tested whether thirst and sodium appetite require angiotensinogen production in astrocytes or hepatocytes. Despite virtually eliminating expression in the brain, deleting astrocytic <jats:italic>Agt<\/jats:italic> did not reduce thirst or sodium appetite. Despite markedly reducing angiotensinogen in the blood, eliminating <jats:italic>Agt<\/jats:italic> from hepatocytes did not reduce thirst or sodium appetite, and in fact, these mice consumed the largest amounts of salt and water after sodium deprivation. Deleting <jats:italic>Agt<\/jats:italic> from both astrocytes and hepatocytes also did not prevent thirst or sodium appetite. Our findings suggest that angiotensin signalling is not required for sodium appetite or thirst and highlight the need to identify alternative signalling mechanisms.\n<jats:boxed-text content-type=\"graphic\" position=\"anchor\"><jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/tjp15628-gra-0001-m.png\"><jats:alt-text>image<\/jats:alt-text><\/jats:graphic><\/jats:boxed-text><\/jats:p><\/jats:sec><jats:sec><jats:title>Key points<\/jats:title><jats:p><jats:list list-type=\"bullet\">\n<jats:list-item><jats:p>Angiotensin signalling is thought to be responsible for the increased thirst and sodium appetite caused by hypovolaemia, producing elevated water and sodium intake.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Specific cells in separate brain regions express the three genes needed to produce angiotensin peptides, but brain\u2010specific deletion of the angiotensinogen gene (<jats:italic>Agt<\/jats:italic>), which encodes the lone precursor for all angiotensin peptides, did not reduce thirst or sodium appetite.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Double\u2010deletion of <jats:italic>Agt<\/jats:italic> from brain and liver also did not reduce thirst or sodium appetite.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Liver\u2010specific deletion of <jats:italic>Agt<\/jats:italic> reduced circulating angiotensinogen levels without reducing thirst or sodium appetite. Instead, these angiotensin\u2010deficient mice exhibited an enhanced sodium appetite.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Because the physiological mechanisms controlling thirst and sodium appetite continued functioning without angiotensin production in the brain and liver, understanding these mechanisms requires a renewed search for the hypovolaemic signals necessary for activating each behaviour.<\/jats:p><\/jats:list-item>\n<\/jats:list><\/jats:p><\/jats:sec>","DOI":"10.1113\/jp283169","type":"journal-article","created":{"date-parts":[[2023,6,9]],"date-time":"2023-06-09T05:10:58Z","timestamp":1686287458000},"page":"3499-3532","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["Sodium appetite and thirst do not require angiotensinogen production in astrocytes or hepatocytes"],"prefix":"10.1113","volume":"601","author":[{"given":"Lila","family":"Peltekian","sequence":"first","affiliation":[{"name":"Department of Neurology University of Iowa Iowa City IA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Silvia","family":"Gasparini","sequence":"additional","affiliation":[{"name":"Department of Neurology University of Iowa Iowa City IA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1941-0435","authenticated-orcid":false,"given":"Frederico S.","family":"Fazan","sequence":"additional","affiliation":[{"name":"Department of Neurology University of Iowa Iowa City IA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Samyukta","family":"Karthik","sequence":"additional","affiliation":[{"name":"Department of Neurology University of Iowa Iowa City IA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gabrielle","family":"Iverson","sequence":"additional","affiliation":[{"name":"Department of Neurology University of Iowa Iowa City IA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jon M.","family":"Resch","sequence":"additional","affiliation":[{"name":"Iowa Neuroscience Institute University of Iowa Iowa City IA USA"},{"name":"Department of Neuroscience and Pharmacology University of Iowa Iowa City IA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9956-4006","authenticated-orcid":false,"given":"Joel C.","family":"Geerling","sequence":"additional","affiliation":[{"name":"Department of Neurology University of Iowa Iowa City IA USA"},{"name":"Iowa Neuroscience Institute University of Iowa Iowa City IA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2023,6,27]]},"reference":[{"key":"e_1_2_5_2_1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00511.2016"},{"key":"e_1_2_5_3_1","doi-asserted-by":"publisher","DOI":"10.1097\/01.hjh.0000166834.32817.41"},{"key":"e_1_2_5_4_1","doi-asserted-by":"publisher","DOI":"10.1159\/000197863"},{"key":"e_1_2_5_5_1","doi-asserted-by":"publisher","DOI":"10.1126\/science.aan6747"},{"key":"e_1_2_5_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/0014-2999(78)90035-3"},{"key":"e_1_2_5_7_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2019.11.040"},{"key":"e_1_2_5_8_1","doi-asserted-by":"publisher","DOI":"10.1002\/cne.902620408"},{"key":"e_1_2_5_9_1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI112130"},{"key":"e_1_2_5_10_1","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000119190.06968.f1"},{"key":"e_1_2_5_11_1","doi-asserted-by":"publisher","DOI":"10.1038\/308206a0"},{"key":"e_1_2_5_12_1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI112566"},{"key":"e_1_2_5_13_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.heliyon.2022.e12221"},{"key":"e_1_2_5_14_1","doi-asserted-by":"publisher","DOI":"10.1161\/hy0202.103441"},{"key":"e_1_2_5_15_1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI88641"},{"key":"e_1_2_5_16_1","doi-asserted-by":"publisher","DOI":"10.1126\/science.6169149"},{"key":"e_1_2_5_17_1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00525.2004"},{"key":"e_1_2_5_18_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.09-05-01668.1989"},{"key":"e_1_2_5_19_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.physbeh.2004.02.013"},{"key":"e_1_2_5_20_1","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1984.sp015359"},{"key":"e_1_2_5_21_1","doi-asserted-by":"publisher","DOI":"10.1016\/0196-9781(82)90113-9"},{"key":"e_1_2_5_22_1","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1970.sp009220"},{"key":"e_1_2_5_23_1","first-page":"953","article-title":"Mice lacking angiotensin\u2010converting enzyme have low blood pressure, renal pathology, and reduced male fertility","volume":"74","author":"Esther C. 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