{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T22:05:30Z","timestamp":1789596330718,"version":"build-2803163510"},"reference-count":37,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"1","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Hypertension"],"published-print":{"date-parts":[[2000,7]]},"abstract":"<jats:p>\n            <jats:italic>Abstract<\/jats:italic>\n            \u2014Blood flow participates  in vascular remodeling during development and growth by regulating cell  apoptosis and proliferation. However, its significance in the  development of vascular hypertrophy and vascular remodeling  in hypertensive patients is not known. We investigated how changing  blood flow through the common carotid artery (CA) of young adult rats  rendered hypertensive via aortic coarctation affects CA  hypertrophy and\/or remodeling responses to hypertension.  Blood flow was reduced by \u224850% as a result of ligation of the  external CA immediately after hypertension was induced, and the effects  of that procedure were compared with those in similarly treated  normotensive rats. Reducing blood flow in the hypertensive animals  markedly augmented the development of CA hypertrophy over  the ensuing 14 days by increasing the vessel wall cross-sectional area.  In those animals, CA lumen size was unaltered by reducing blood flow,  as was CA structure in normotensive animals. The greater  hypertrophy in the hypertensive animals with reduced blood  flow was associated with enhanced smooth muscle cell (SMC)  proliferation 3 days after the hemodynamic changes were  induced. There also appeared to be more extensive remodeling of the  endothelium in the hypertensive animals with normal  flow; this was indicated by the greater frequency of apoptotic  endothelial cells at that time. This reduction in blood  flow also attenuated endothelial cell nitric oxide  synthase expression in hypertensive animals but not in normotensive  animals. Severe reductions in blood flow (\u224890%) were required to  reduce endothelial cell nitric oxide synthase in the  normotensive animals. Increasing CA nitric oxide levels by  perivascular application of\n            <jats:italic>S<\/jats:italic>\n            -nitroso-\n            <jats:italic>N<\/jats:italic>\n            -acetylpenicillamine (SNAP) to  the CAs of hypertensive animals with reduced  endothelial cell nitric oxide synthase attenuated the  greater SMC proliferation. Thus, reduced blood flow in hypertensive  animals promotes hypertrophy by enhancing SMC proliferation  via mechanisms that reduce the inhibitory effects of nitric  oxide on SMC proliferation.\n          <\/jats:p>","DOI":"10.1161\/01.hyp.36.1.89","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:25:31Z","timestamp":1339460731000},"page":"89-96","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":38,"title":["Blood Flow Regulates the Development of Vascular Hypertrophy, Smooth Muscle Cell Proliferation, and Endothelial Cell Nitric Oxide Synthase in Hypertension"],"prefix":"10.1161","volume":"36","author":[{"given":"Hitoshi","family":"Ueno","sequence":"first","affiliation":[{"name":"From the Cell Biology Laboratory, Baker Medical Research Institute and  Alfred Hospital, Melbourne, VIC, Australia."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter","family":"Kanellakis","sequence":"additional","affiliation":[{"name":"From the Cell Biology Laboratory, Baker Medical Research Institute and  Alfred Hospital, Melbourne, VIC, Australia."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alex","family":"Agrotis","sequence":"additional","affiliation":[{"name":"From the Cell Biology Laboratory, Baker Medical Research Institute and  Alfred Hospital, Melbourne, VIC, Australia."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alex","family":"Bobik","sequence":"additional","affiliation":[{"name":"From the Cell Biology Laboratory, Baker Medical Research Institute and  Alfred Hospital, Melbourne, VIC, Australia."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_1_1_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.hyp.21.4.391"},{"key":"e_1_3_1_2_2","doi-asserted-by":"crossref","unstructured":"Korner PI Angus JA Bobik A Jennings GL. 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