INFLUENCE OF CARBON MONOXIDE DONOR ON VASCULAR SMOOTH MUSCLES CONTRACTILE FUNCTION UNDER NORMOXIA AND HYPOXIA

Abstract

Carbon monoxide (CO) belongs to a family of gasotransmitters. It is an important signaling molecule that involved in a wide range of physiological processes in the organism, including the mechanisms of regulation of vascular smooth muscle contractile activity. It is known that contractile function of vascular smooth muscle cells (VSMC) may change in different pathological processes , like as hypoxia. In this case the modification of gaseous communication will occur. The aim of this study was to investigate the CO donor (tricarbonyldichlororuthenium (II)-dimer, CORM II) influence on the contractile properties of VSMC under normoxia and hypoxia . Obtained data show that under normoxia, CORM II induces relaxation of vascular smooth muscle segments, precontracted both with highpotassium solution and phenylephrine (PE, 1 μM). Moreover, in PE-induced contraction, the concentration of CORM II providing a half-maximal relaxing effect was significantly lower than under the action of high potassium solution (10 and 100 μM, respectively). The blocker of potassium channels – tetraethylammonium (TEA, 10 mM) led to decrease of the CO-induced relaxation. Therefore, we can conclude that the mechanism of CO action on the smooth muscles contractile activity is associated with an increase of potassium conductance of VSMC membranes. Under hypoxic conditions, the relaxing effect of CO was decreased both in high potassium- and PE- precontracted smooth muscle segments, but in varying degrees. This may be due to a more intense inhibitory effect of hypoxia on the one of the components of the membrane potassium conductance and /or other intracellular targets of CO.