Effects of hyperbaric oxygenation on vascular reactivity to angiotensin II and angiotensin-(1-7) in rats

Objective: To assess and elucidate the mechanisms of hyperbaric oxygenation (HBO₂) effects on vascular reactivity to angiotensin-(1-7) [ANG-(1-7)] and angiotensin II (ANG II). Methods: Rat aortic rings (HBO ₂ vs. control group) were used to test responses to ANG II, ANG II+ ANG-(1-7) or ANG-(1-7) after noradrenaline precontraction in the presence/absence of MS-PPOH, a specific CYP 450-epoxygenase inhibitor, and glibenclamide, a K_{AT P} channels inhibitor. mRNA expression studies of specific CYP isozymes have been conducted as well. Results: The mean contraction (expressed as percent of maximal contraction) for ANG II was similar between groups. Contraction for ANG II + ANG-(1-7) was 15% ± 10 (HBO₂) and 20% ± 9 (control). There was a significant decrease between the contraction response to ANG II (HBO₂) and the response to ANG II + ANG-(1-7) in the HBO₂ group, without such a difference within the control group. Mean percentage of noradrenaline precontraction decrease after ANG-(1-7) addition was significantly different [10% ± 9 (control) and 19% ± 11 (HBO₂)]. The epoxygenase inhibitor MS-PPOH in HBO₂ animals reversed these changes. Glibenclamide had no effect on relaxation in response to ANG-(1-7). Expression of CYP4A2, CYP4A3 and CYP2J3 mRNA was not significantly altered with HBO, whereas CYP4A1 was significantly upregulated. Conclusions: Our results suggest a role for epoxyeicosatrienoic acids in modulating relaxation response to ANG-(1-7) with HBO₂ that is conducted via potassium channels other than K _{AT P} channels. HBO₂ increased the responses to ANG-(1-7) after precontraction with noradrenaline. The difference between the response to ANG II in the HBO₂ group and ANG II + ANG-(1-7) in the HBO ₂ group (the contraction force of the peptide combination being lower), without such difference in the control group, suggests an influence of HBO₂ on vascular reactivity.