Objectives: The aim of this study is to determine the role of TRP ion channels in mechanism of flow-induced dilation and the impact of acute and intermittent hyperbaric oxygenation on activity of TRP ion channels in mechanism of flow-induced dilation. Study design: Experimental study on laboratory animals Materials and methods: Healthy SD rats (N=24) were divided into 3 groups – control (CTRL, N=12), A-HBOT (N=6) and 4D-HBOT (N=6). A-HBOT group was subjected to acute HBO2 in specialized chamber (100% O2, 2h/2bars) and 4D-HBOT group was exposed to intermittent HBO2 (exposure for 4 days in a row). After the protocol, rats were anesthetized (ketamine – 75mg/kg, midazolam – 0,5 mg/kg) and subsequently decapitated, MCA was isolated and incubated for 1 hour in the pressure myograph system (where P1 was Δ80 mmHg and P2 Δ0 mmHg) so that basal diameter can be measured. The vessel was exposed to the flow of PSS solution. The basal values of the vessel diameter and the response of the vessel to individual agonists (GSK1016790A, 300nM/L, Sigma Aldrich) and antagonists (RN-1734, 20μM/L, Sigma Aldrich) at pressure gradients were measured. After the basal response, FID of the vessels of the control group in presence of antagonist and agonist of TRPV4 channel, FID of vessles of A-HBOT group in the presence of agonist and the FID of vessles of 4D-HBOT group in the presence of antagonist were measured. The PSS eventually changes to PSS Ca-free for the purpose of measuring the maximum artery diameter. Results: In the control group, use of RN-1734 led to a decrease in FID at each of the pressure gradients and GSK1016790A led to an increase in FID at level of Δ40 mmHg, Δ60 mmHg i Δ100 mmHg pressure gradients according to basal values. The FID of the A-HBOT group with the agonist applied was significantly restored at the level of Δ40, Δ60 i Δ100 mmHg pressure gradients according to the basal response of the untreated A-HBOT group (FID disrupted). Application of antagonist in the 4D-HBOT group disrupted FID at the level of Δ20, Δ40, Δ60 i Δ100 mmHg pressure gradients according to the basal response of the untreated 4D-HBOT group (FID preserved). Conclusion: TRP ion channels play a significant role in basal mediation of flow-induced dilatation, and in mediation of FID after acute and intermittent exposure to hyperbaric oxygenation