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However, studies in the literature, reviewed here, provide substantial support for such direct targets. Twenty\u2010three studies have shown that voltage\u2010gated calcium channels (<jats:styled-content style=\"fixed-case\">VGCC<\/jats:styled-content>s) produce these and other <jats:styled-content style=\"fixed-case\">EMF<\/jats:styled-content> effects, such that the L\u2010type or other <jats:styled-content style=\"fixed-case\">VGCC<\/jats:styled-content> blockers block or greatly lower diverse <jats:styled-content style=\"fixed-case\">EMF<\/jats:styled-content> effects. Furthermore, the voltage\u2010gated properties of these channels may provide biophysically plausible mechanisms for <jats:styled-content style=\"fixed-case\">EMF<\/jats:styled-content> biological effects. Downstream responses of such <jats:styled-content style=\"fixed-case\">EMF<\/jats:styled-content> exposures may be mediated through <jats:styled-content style=\"fixed-case\"><jats:roman>Ca<jats:sup>2+<\/jats:sup><\/jats:roman><\/jats:styled-content>\/calmodulin stimulation of nitric oxide synthesis. Potentially, physiological\/therapeutic responses may be largely as a result of nitric oxide\u2010<jats:styled-content style=\"fixed-case\">cGMP<\/jats:styled-content>\u2010protein kinase G pathway stimulation. A well\u2010studied example of such an apparent therapeutic response, <jats:styled-content style=\"fixed-case\">EMF<\/jats:styled-content> stimulation of bone growth, appears to work along this pathway. However, pathophysiological responses to <jats:styled-content style=\"fixed-case\">EMF<\/jats:styled-content>s may be as a result of nitric oxide\u2010peroxynitrite\u2010oxidative stress pathway of action. A single such well\u2010documented example, <jats:styled-content style=\"fixed-case\">EMF<\/jats:styled-content> induction of <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content> single\u2010strand breaks in cells, as measured by alkaline comet assays, is reviewed here. Such single\u2010strand breaks are known to be produced through the action of this pathway. Data on the mechanism of <jats:styled-content style=\"fixed-case\">EMF<\/jats:styled-content> induction of such breaks are limited; what data are available support this proposed mechanism. Other <jats:styled-content style=\"fixed-case\"><jats:roman>Ca<jats:sup>2+<\/jats:sup><\/jats:roman><\/jats:styled-content>\u2010mediated regulatory changes, independent of nitric oxide, may also have roles. This article reviews, then, a substantially supported set of targets, <jats:styled-content style=\"fixed-case\">VGCC<\/jats:styled-content>s, whose stimulation produces non\u2010thermal <jats:styled-content style=\"fixed-case\">EMF<\/jats:styled-content> responses by humans\/higher animals with downstream effects involving <jats:styled-content style=\"fixed-case\"><jats:roman>Ca<jats:sup>2+<\/jats:sup><\/jats:roman><\/jats:styled-content>\/calmodulin\u2010dependent nitric oxide increases, which may explain therapeutic and pathophysiological effects.<\/jats:p>","DOI":"10.1111\/jcmm.12088","type":"journal-article","created":{"date-parts":[[2013,6,27]],"date-time":"2013-06-27T04:34:19Z","timestamp":1372307659000},"page":"958-965","source":"Crossref","is-referenced-by-count":396,"title":["Electromagnetic fields act <i>via<\/i> activation of voltage\u2010gated calcium channels to produce beneficial or adverse effects"],"prefix":"10.1111","volume":"17","author":[{"given":"Martin 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