{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,31]],"date-time":"2026-07-31T02:56:48Z","timestamp":1785466608280,"version":"3.56.0"},"reference-count":67,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2021,3,28]],"date-time":"2021-03-28T00:00:00Z","timestamp":1616889600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"DOI":"10.13039\/501100001230","name":"Macquarie University","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001230","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Hillcrest Foundation"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2022,3,16]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aims<\/jats:title>\n                    <jats:p>Hypertension is a prevalent yet poorly understood feature of polycystic kidney disease. Previously, we demonstrated that increased glutamatergic neurotransmission within the hypothalamic paraventricular nucleus produces hypertension in the Lewis Polycystic Kidney (LPK) rat model of polycystic kidney disease. Here, we tested the hypothesis that augmented glutamatergic drive to the paraventricular nucleus in Lewis polycystic kidney rats originates from the forebrain lamina terminalis, a sensory structure that relays blood-borne information throughout the brain.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and results<\/jats:title>\n                    <jats:p>Anatomical experiments revealed that 38% of paraventricular nucleus-projecting neurons in the subfornical organ of the lamina terminalis expressed Fos\/Fra, an activation marker, in LPK rats while &amp;lt;1% of neurons were Fos\/Fra+ in Lewis control rats (P\u00a0=\u00a00.01, n\u00a0=\u00a08). In anaesthetized rats, subfornical organ neuronal inhibition using isoguvacine produced a greater reduction in systolic blood pressure in LPK vs. Lewis rats (\u221221\u00b14 vs. \u22127\u00b12\u00a0mmHg, P\u00a0&amp;lt;\u00a00.01; n\u00a0=\u00a010), which could be prevented by prior blockade of paraventricular nucleus ionotropic glutamate receptors using kynurenic acid. Blockade of ionotropic glutamate receptors in the paraventricular nucleus produced an exaggerated depressor response in LPK relative to Lewis rats (\u221223\u00b14 vs. \u22122\u00b13\u00a0mmHg, P\u00a0&amp;lt;\u00a00.001; n\u00a0=\u00a013), which was corrected by prior inhibition of the subfornical organ with muscimol but unaffected by chronic systemic angiotensin II type I receptor antagonism or lowering of plasma hyperosmolality through high-water intake (P\u00a0&amp;gt;\u00a00.05); treatments that both nevertheless lowered blood pressure in LPK rats (P\u00a0&amp;lt;\u00a00.0001).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Our data reveal multiple independent mechanisms contribute to hypertension in polycystic kidney disease, and identify high plasma osmolality, angiotensin II type I receptor activation and, importantly, a hyperactive subfornical organ to paraventricular nucleus glutamatergic pathway as potential therapeutic targets.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/cvr\/cvab122","type":"journal-article","created":{"date-parts":[[2021,3,26]],"date-time":"2021-03-26T08:10:10Z","timestamp":1616746210000},"page":"1138-1149","source":"Crossref","is-referenced-by-count":2,"title":["The subfornical organ drives hypertension in polycystic kidney disease via the hypothalamic paraventricular nucleus"],"prefix":"10.1093","volume":"118","author":[{"given":"Conor F","family":"Underwood","sequence":"first","affiliation":[{"name":"Department of Biomedical Sciences, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney, NSW 2109, Australia"},{"name":"Department of Anatomy, School of Biomedical Sciences, University of Otago, Dunedin 9016, New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Simon","family":"McMullan","sequence":"additional","affiliation":[{"name":"Department of Biomedical Sciences, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney, NSW 2109, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ann K","family":"Goodchild","sequence":"additional","affiliation":[{"name":"Department of Biomedical Sciences, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney, NSW 2109, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4917-7734","authenticated-orcid":false,"given":"Jacqueline K","family":"Phillips","sequence":"additional","affiliation":[{"name":"Department of Biomedical Sciences, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney, NSW 2109, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6468-8922","authenticated-orcid":false,"given":"Cara M","family":"Hildreth","sequence":"additional","affiliation":[{"name":"Department of Biomedical 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