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Both short\u2010term (30\u2009min) and prolonged (24\u2009h) treatment with Ang II increased reactive oxygen species (ROS) production through NADPH oxidase (NOX) activation, with increased phosphorylation of PKC\u03b2 at active site Ser660 in rat primary VSMCs from mesenteric artery. The increases in ROS production and NOX activity were completely abolished in VSMCs of PKC\u03b2\u2010knockout rats, in which the absence of PKC\u03b2 mRNA expression was confirmed. Genomic and pharmacologic analyses indicated that prolonged treatment with Ang II increased ROS production via NF\u2010\u03baB\u2013mediated NOX1 and p22\n                    <jats:sup>phox<\/jats:sup>\n                    expression via the PKC\u03b2\/ROS pathway. In\u00a0vivo infusion of Ang II at a low dose (10\u2009ng\/kg\/min) for 7\u2009days increased ROS production and NOX1 and p22\n                    <jats:sup>phox<\/jats:sup>\n                    expression in mesenteric artery in both male and female non\u2010transgenic rats, and these effects were abolished by PKC\u03b2 gene deletion. These results suggest that the PKC\u03b2 isoform is the primary regulator of oxidative stress in VSMCs in response to both acute and subacute exposure to Ang II.\n                  <\/jats:p>","DOI":"10.14814\/phy2.70595","type":"journal-article","created":{"date-parts":[[2025,10,17]],"date-time":"2025-10-17T06:07:29Z","timestamp":1760681249000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Critical role of the \u03b2 isoform of protein kinase C (\n                    <scp>PKC\u03b2<\/scp>\n                    ) in angiotensin\n                    <scp>II<\/scp>\n                    \u2013induced oxidative stress in vascular smooth muscle cells"],"prefix":"10.14814","volume":"13","author":[{"given":"Hirotaka","family":"Tajima","sequence":"first","affiliation":[{"name":"Laboratory of Veterinary Pharmacology, Faculty of Veterinary Medicine Okayama University of Science  Imabari Ehime 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