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Carbon monoxide (CO) is one of a family of gas transmitters. In this article, we present the results of mechanographic investigations of the mechanisms of CO action on rat thoracic aorta segments. We have found that relaxing effect of CORM-2, CO donor, on vascular smooth muscles was mediated mainly by opening of voltage-gated potassium channels in smooth muscle cells: 4-aminopyridine, blocking these channels, almost completely eliminated CO-induced vasorelaxation of the segments precontracted by depolarization of the smooth muscle cell membranes with high potassium (30 mM KCl) solution or by phenylephrine (10 mM). For the first time, we have documented that CORM-2 reduces the nicardipine-sensitive input of45 Ca2+ in freshly isolated aorta cells. There are reasons to suppose that the L-type voltage-gated calcium channels of the vascular smooth muscle cells are another CO target for the relaxing effect of this gas transmitter. Additional studies are required to determine the influence of ruthenium complexes (Ru(II)) on phenomenology of carbon monoxide effects.