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We tested the hypothesis that CAII catalyses NO formation from nitrite and contributes to nitrite\u2010dependent inhibition of platelet activation and vasodilation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Experiment approach<\/jats:title><jats:p>The role of CAII in enzymatic NO generation was investigated by measuring NO formation from the reaction of isolated human and bovine CAII with nitrite using NO photolysis\u2010chemiluminescence. A CAII\u2010deficient mouse model was used to determine the role of CAII in red blood cell mediated nitrite reduction and vasodilation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Key results<\/jats:title><jats:p>We found that the commercially available purified bovine CAII exhibited limited and non\u2010enzymatic NO\u2010generating reactivity in the presence of nitrite with or without addition of the CA inhibitor dorzolamide; the NO formation was eliminated with purification of the enzyme. There was no significant detectable NO production from the reaction of nitrite with recombinant human CAII. Using a CAII\u2010deficient mouse model, there were no measurable changes in nitrite\u2010dependent vasodilation in isolated aorta rings and in vivo in CAII<jats:sup>\u2212\/\u2212<\/jats:sup>, CAII<jats:sup>+\/\u2212<\/jats:sup>, and wild\u2010type mice. Moreover, deletion of the CAII gene in mice did not block nitrite reduction by red blood cells and the nitrite\u2010NO\u2010dependent inhibition of platelet activation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion and implications<\/jats:title><jats:p>These studies suggest that human, bovine and mouse CAII are not responsible for nitrite\u2010dependent NO formation in red blood cells, aorta, or the systemic circulation.<\/jats:p><\/jats:sec>","DOI":"10.1111\/bph.14887","type":"journal-article","created":{"date-parts":[[2019,10,28]],"date-time":"2019-10-28T17:48:41Z","timestamp":1572284921000},"page":"898-911","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["Carbonic anhydrase II does not regulate nitrite\u2010dependent nitric oxide formation and vasodilation"],"prefix":"10.1111","volume":"177","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4333-3158","authenticated-orcid":false,"given":"Ling","family":"Wang","sequence":"first","affiliation":[{"name":"Pittsburgh Heart, Lung, Blood and Vascular Medicine Institute University of Pittsburgh  Pittsburgh Pennsylvania"},{"name":"Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine University of Pittsburgh  Pittsburgh Pennsylvania"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2954-9633","authenticated-orcid":false,"given":"Courtney E.","family":"Sparacino\u2010Watkins","sequence":"additional","affiliation":[{"name":"Pittsburgh Heart, Lung, Blood and Vascular Medicine Institute University of Pittsburgh  Pittsburgh Pennsylvania"},{"name":"Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine University of Pittsburgh  Pittsburgh Pennsylvania"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jun","family":"Wang","sequence":"additional","affiliation":[{"name":"Hubei University of Technology  Wuhan P. 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