The increase in intracellular Ca²⁺ is a key stimulus for contraction of vascular smooth muscle (VSM). Along with that, a number of intracellular signaling pathways sustain contraction without additional rise of in Ca²⁺, thereby providing Ca²⁺-sensitisation of the contraction. Earlier our colleagues demonstrated that Ca²⁺-sensitivity of VSM contraction in newborn rats is higher than in adults, but the mechanism of such phenomenon has not been explored. Mitogen-activated protein kinases (MAPK) are the molecules that take part in Ca²⁺- sensitisation of VSM contraction. We investigated the role of two members of MAPK family (ERK1/2 and p38) in saphenous artery of 2-week-old (2WK) and adult (AD) rats. For this purpose we studied the effects of ERK1/2 and p38 inhibition with U0126 and SB202190 respectively (10^-5 M for both) on isometric contractile response to methoxamine (selective a1-adrenoceptor agonist). The effect of SB202190 was greater compared with U0126 and more prominent in 2WK than in AD. Together, the inhibitors decreased maximal force in 2WK by about 70 % and in AD only by about 30 %. As the second step we studied the degree of MAPK phosphorylation in relaxed state and after contraction with methoxamine (10–5 M). The segments were snap-frozen in liquid N2 and homogenized. Proteins separated with SDS-PAGE were transferred to PVDF membranes. Membranes were incubated with anti-MAPK and anti-phospho- MAPK antibodies and then visualized with enhanced chemiluminescence. The degree of MAPK phosphorylation was nearly the same in 2WK and AD, but total MAPK content in 2WK was greatly higher than in AD (3-fold for ERK1/2 and 5-fold for p38). We suggest that ERK1/2 and p38 pathways are more important for VSM contraction in young rats and may take part in Ca²⁺-sensitisation.