{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,26]],"date-time":"2026-06-26T21:49:38Z","timestamp":1782510578297,"version":"3.54.5"},"reference-count":30,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2025,2,17]],"date-time":"2025-02-17T00:00:00Z","timestamp":1739750400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2025,2,17]],"date-time":"2025-02-17T00:00:00Z","timestamp":1739750400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/100010269","name":"Wellcome Trust","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100010269","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000274","name":"British Heart Foundation","doi-asserted-by":"publisher","award":["AA\/18\/1\/34219"],"award-info":[{"award-number":["AA\/18\/1\/34219"]}],"id":[{"id":"10.13039\/501100000274","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100016133","name":"James Tudor Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100016133","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":[[2025,3]]},"abstract":"<jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>\n                      Adults with hypertension have higher prevalence of vertebral artery hypoplasia (VAH), which is associated with lower resting cerebral blood flow (CBF). We examined whether VAH impacts the ability to regulate CBF during haemodynamic stress when cardiac output and blood pressure are lowered via body negative pressure (LBNP). Participants underwent magnetic resonance angiography (MRA) at 1.5T during LBNP at 0, \u221220 and \u221240\u00a0mmHg, and were assigned to VAH (\n                      <jats:italic>n<\/jats:italic>\n                      \u00a0=\u00a013) or without\u2010VAH (\n                      <jats:italic>n<\/jats:italic>\n                      \u00a0=\u00a011) groups post\u2010acquisition. Phase\u2010contrast MRA measured flow in the basilar artery (BA), internal carotid arteries (ICA), and the ascending aorta to measure cardiac output (CO). The CO decreased during all levels of LBNP in both groups (LBNP main effect\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0&lt;\u00a00.0001), whereas MAP was reduced in the group without VAH only (\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0=\u00a00.0003). BA flow was reduced during LBNP in the group without VAH (\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0=\u00a00.0267 at \u221220\u00a0mmHg and\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0&lt;\u00a00.0001 at \u221240\u00a0mmHg) but was surprisingly unchanged in the group with VAH (\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0&gt;\u00a00.05 all levels LBNP). ICA flow decreased during LBNP (\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0&lt;\u00a00.0001) and was not different between groups. Total CBF decreased during LBNP in hypertensives without VAH (\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0=\u00a00.0192 at \u221220\u00a0mmHg and\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0&lt;\u00a00.0001 at \u221240\u00a0mmHg) but was unchanged in patients with VAH (\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0&gt;\u00a00.05 at all levels of LBNP). Total peripheral resistance (TPR) increased during LBNP in both groups, but the rise was greater in the group with VAH (\u221220\u00a0mmHg;\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0=\u00a00.0129, \u201340\u00a0mmHg;\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0=\u00a00.0016). In summary, hypertensive patients without VAH may tolerate decreases in CBF, whereas patients with VAH evoke a greater systemic TPR response to preserve CBF.\n                      <jats:boxed-text content-type=\"graphic\" position=\"anchor\">\n                        <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/tjp16570-gra-0001-m.png\">\n                          <jats:alt-text>image<\/jats:alt-text>\n                        <\/jats:graphic>\n                      <\/jats:boxed-text>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key points<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>Vertebral artery hypoplasia (VAH) is more common in hypertensive adults and is associated with lower resting cerebral blood flow (CBF), suggesting that VAH might impair the brain's ability to maintain cerebral blood flow during haemodynamic stress using lower body negative pressure.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>This study shows that hypertensive patients with VAH maintain CBF during body negative pressure, unlike those without VAH, who experience reductions in CBF. Patients with VAH show a greater rise in total peripheral resistance (TPR), suggesting a compensatory mechanism to maintain cerebral perfusion.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>The findings highlight that patients with VAH have an altered physiological response to hypovolaemia, where they may rely on systemic pressor responses to maintain perfusion of posterior brain territories in already hypoperfused circulation.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>This is important for understanding how VAH impacts cerebrovascular function in hypertensive patients and may influence clinical approaches to managing CBF in disease conditions.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1113\/jp287786","type":"journal-article","created":{"date-parts":[[2025,2,17]],"date-time":"2025-02-17T10:30:21Z","timestamp":1739788221000},"page":"1417-1437","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Cerebral blood flow during simulated central hypovolaemia in people with hypertension: does vertebral artery hypoplasia matter?"],"prefix":"10.1113","volume":"603","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7306-9047","authenticated-orcid":false,"given":"Sandra","family":"Neumann","sequence":"first","affiliation":[{"name":"School of Physiology, Pharmacology and Neuroscience University of Bristol  Bristol UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jonathan C. L.","family":"Rodrigues","sequence":"additional","affiliation":[{"name":"Department of Radiology Royal United Hospitals Bath NHS Foundation Trust  UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lydia L.","family":"Simpson","sequence":"additional","affiliation":[{"name":"School of Physiology, Pharmacology and Neuroscience University of Bristol  Bristol UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chris B.","family":"Lawton","sequence":"additional","affiliation":[{"name":"Department of Cardiology University Hospitals Bristol and Weston NHS Foundation Trust  UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel","family":"Burden","sequence":"additional","affiliation":[{"name":"Department of Cardiology University Hospitals Bristol and Weston NHS Foundation Trust  UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthew D.","family":"Kobetic","sequence":"additional","affiliation":[{"name":"School of Physiology, Pharmacology and Neuroscience University of Bristol  Bristol UK"},{"name":"Department of Cardiology University Hospitals Bristol and Weston NHS Foundation Trust  UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0187-0123","authenticated-orcid":false,"given":"Zoe H.","family":"Adams","sequence":"additional","affiliation":[{"name":"School of Physiology, Pharmacology and Neuroscience University of Bristol  Bristol UK"},{"name":"Cardiff School of Sport and Health Sciences Cardiff Metropolitan University  Cardiff UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katrina","family":"Hope","sequence":"additional","affiliation":[{"name":"School of Physiology, Pharmacology and Neuroscience University of Bristol  Bristol UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7410-2913","authenticated-orcid":false,"given":"Julian F. R.","family":"Paton","sequence":"additional","affiliation":[{"name":"Manaaki Manawa, The Centre for Heart Research University of Auckland  Auckland New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hazel","family":"Blythe","sequence":"additional","affiliation":[{"name":"School of Physiology, Pharmacology and Neuroscience University of Bristol  Bristol UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5366-5992","authenticated-orcid":false,"given":"Nathan","family":"Manghat","sequence":"additional","affiliation":[{"name":"Department of Cardiology University Hospitals Bristol and Weston NHS Foundation Trust  UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6317-4153","authenticated-orcid":false,"given":"Jill N.","family":"Barnes","sequence":"additional","affiliation":[{"name":"Department of Kinesiology, Bruno Balke Biodynamics Laboratory University of Wisconsin\u2010Madison  Madison WI USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9435-726X","authenticated-orcid":false,"given":"Angus K.","family":"Nightingale","sequence":"additional","affiliation":[{"name":"School of Physiology, Pharmacology and Neuroscience University of Bristol  Bristol UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0474-4598","authenticated-orcid":false,"given":"Mark C. 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