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High salt diet-induced alteration in vascular reactivity in wild-type and adenosine A2A receptor null mice Isha Pradhan Alteration in vascular reactivity serves as a marke r for cardiovascular disease. Enhancement of vasodilatory response through adenos ine A2A receptor (A2AAR) signaling against high salt (HS) diet is speculated to be an adaptive response as salt-sensitive rats showed upregulation of A2AAR and cyp-epoxygenases but salt-resistant rats did not. However, no direct evidence is available showing th e compensatory role of A 2 AR signaling upon salt loading. For this, understandin g the functional and biochemical outcome of HS diet on vascular tone regulation and its underlying signaling mechanism in the presence and absence of A 2AAR is required. This dissertation was carried out t o investigate the role of A 2AAR and epoxyeicosatrienoic acid (EETs) on HS-modula ted vascular reactivity and its signaling pathway invol ved using A2AAR +/+ and A2AAR -/mice. Isometric tension measurement and western blot stud ies were conducted to evaluate aortic reactivity and underlying signaling mechanis m in HS and normal salt (NS) fed A2AAR +/+ and A2AAR -/mice. Our data demonstrated clear differences in v ascular reactivity and their signaling mechanism between A 2AAR +/+ and A2AAR -/mice on a HS diet. HS diet enhanced vascular relaxation to adeno sine in A2AAR +/+ mice, while HS diet amplified contraction to adenosine in A 2A R -/mice. In the presence of A 2 AR, we found that enhanced vascular relaxation to HS is mediated through A2AAR coupled with EETs that activate peroxisome proliferator activated rec eptor-gamma (PPAR γ) leading to opening of ATP-sensitive K+ (K ATP) channels downstream. In contrary, in the absence o f A2AAR, HS-elicited amplified contraction is found to o ccur through loss of vasodilatory response and its signaling involving EETs and PPAR γ and increased vasoconstrictors such as adenosine A 1 receptor (A1AR) and soluble epoxide hydrolase (sEH), an enzyme that degrades EETs. Most importantly, our finding r evealed that increasing EETs availability through sEH inhibition could be a pote ntial strategy to improve exaggerated vascular contraction in HS-fed A 2 AR -/mice.