{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T18:58:17Z","timestamp":1791917897984,"version":"4.3.4"},"reference-count":55,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2022,2,15]]},"abstract":"<jats:sec xml:lang=\"en\">\n                    <jats:title>Background<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      Blood pressure and tissue perfusion are controlled in part by the level of intrinsic (myogenic) arterial tone. However, many of the molecular determinants of this response are unknown. We previously found that mice with targeted disruption of the gene encoding the angiotensin II type 1a receptor (AT1AR) (\n                      <jats:italic>Agtr1a<\/jats:italic>\n                      ), the major murine angiotensin II type 1 receptor (AT1R) isoform, showed reduced myogenic tone; however, uncontrolled genetic events (in this case, gene ablation) can lead to phenotypes that are difficult or impossible to interpret.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Methods and Results<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      We tested the mechanosensitive function of AT1R using tamoxifen\u2010inducible smooth muscle\u2010specific AT1aR knockout (smooth muscle\u2010\n                      <jats:italic>Agtr1a<\/jats:italic>\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      ) mice and studied downstream signaling cascades mediated by G\n                      <jats:sub>q\/11<\/jats:sub>\n                      and\/or \u03b2\u2010arrestins. FR900359, Sar1Ile4Ile8\u2010angiotensin II (SII), TRV120027 and TRV120055 were used as selective G\n                      <jats:sub>q\/11<\/jats:sub>\n                      inhibitor and biased agonists to activate noncanonical \u03b2\u2010arrestin and canonical G\n                      <jats:sub>q\/11<\/jats:sub>\n                      signaling of the AT1R, respectively. Myogenic and Ang II\u2010induced constrictions were diminished in the perfused renal vasculature, mesenteric and cerebral arteries of smooth muscle\u2010\n                      <jats:italic>Agtr1a<\/jats:italic>\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      mice. Similar effects were observed in arteries of global mutant\n                      <jats:italic>Agtr1a<\/jats:italic>\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      but not\n                      <jats:italic>Agtr1b<\/jats:italic>\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      mice. FR900359 decreased myogenic tone and angiotensin II\u2010induced constrictions whereas selective biased targeting of AT1R\u2010\u03b2\u2010arrestin signaling pathways had no effects.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      This study demonstrates that myogenic arterial constriction requires G\n                      <jats:sub>q\/11<\/jats:sub>\n                      \u2010dependent signaling pathways of mechanoactivated AT1R but not G protein\u2010independent, noncanonical pathways in smooth muscle cells.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/jaha.121.022070","type":"journal-article","created":{"date-parts":[[2022,2,8]],"date-time":"2022-02-08T06:21:54Z","timestamp":1644301314000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":30,"title":["Myogenic Vasoconstriction Requires Canonical G\n                    <sub>q\/11<\/sub>\n                    Signaling of the Angiotensin II Type 1 Receptor"],"prefix":"10.1161","volume":"11","author":[{"given":"Yingqiu","family":"Cui","sequence":"first","affiliation":[{"name":"Experimental and Clinical Research Center (ECRC) a joint cooperation between the Charit\u00e9 Medical Faculty and the Max Delbr\u00fcck Center for Molecular Medicine (MDC) Charit\u00e9 \u2010 Universit\u00e4tsmedizin Berlin Berlin Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4785-6530","authenticated-orcid":false,"given":"Mario","family":"Kassmann","sequence":"additional","affiliation":[{"name":"Experimental and Clinical Research Center (ECRC) a joint cooperation between the Charit\u00e9 Medical Faculty and the Max Delbr\u00fcck Center for Molecular Medicine (MDC) Charit\u00e9 \u2010 Universit\u00e4tsmedizin Berlin Berlin Germany"},{"name":"Department of Internal Medicine and Geriatrics University Medicine Greifswald Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sophie","family":"Nickel","sequence":"additional","affiliation":[{"name":"Experimental and Clinical Research Center (ECRC) a joint cooperation between the Charit\u00e9 Medical Faculty and the Max Delbr\u00fcck Center for Molecular Medicine (MDC) Charit\u00e9 \u2010 Universit\u00e4tsmedizin Berlin Berlin Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chenglin","family":"Zhang","sequence":"additional","affiliation":[{"name":"Heart and Vascular Institute and School of Biomedical Sciences Chinese University of Hong Kong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6071-5433","authenticated-orcid":false,"given":"Natalia","family":"Alenina","sequence":"additional","affiliation":[{"name":"Max Delbr\u00fcck Center for Molecular Medicine Berlin Germany"},{"name":"DZHK (German Center for Cardiovascular Research), Partner Site Berlin Berlin Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoland Marie","family":"Anistan","sequence":"additional","affiliation":[{"name":"Experimental and Clinical Research Center (ECRC) a joint cooperation between the Charit\u00e9 Medical Faculty and the Max Delbr\u00fcck Center for Molecular Medicine (MDC) Charit\u00e9 \u2010 Universit\u00e4tsmedizin Berlin 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Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Donald G.","family":"Welsh","sequence":"additional","affiliation":[{"name":"Department of Physiology and Pharmacology Robarts, Research Institute Western University London Ontario Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1277-6784","authenticated-orcid":false,"given":"Yu","family":"Huang","sequence":"additional","affiliation":[{"name":"Heart and Vascular Institute and School of Biomedical Sciences Chinese University of Hong Kong China"},{"name":"Department of Biomedical Sciences Campus VirchowCity University of Hong Kong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2797-1934","authenticated-orcid":false,"given":"Maik","family":"Gollasch","sequence":"additional","affiliation":[{"name":"Experimental and Clinical Research Center (ECRC) a joint cooperation between the Charit\u00e9 Medical Faculty and 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