Proceedings of The Physiological Society

University of Oxford (2011) Proc Physiol Soc 23, PC229

Poster Communications

Effects of hyperbaric oxygen therapy on reactivity of rat aortic rings to angiotensin II and angiotensin-(1-7)

A. Kibel1, A. Cavka1, I. Drenjancevic1

1. Department of Physiology and Immunology, School of Medicine Osijek, University Josip Juraj Strossmayer in Osijek, Osijek, Croatia.

INTRODUCTION: Hyperbaric oxygen therapy (HBOT) has various effects on perfusion and vascular function and it has been hypothesized that HBOT may change vascular sensitivity to different dilators and constrictors [1]. Angotensin-(1-7) (ANG-(1-7))has been demonstrated to have dilating activity, in contrast to angiotensin II (ANG II) [2]; both peptides having complex mechanisms of action. The aim of our study was to assess whether there are effects of HBOT on vascular reactivity to ANG II and ANG-(1-7). METHODS: Thoracic aortic ring preparations from Sprague-Dawley rats, divided into an HBOT and a control group, were used to test responses to ANG II, ANG II+ ANG-(1-7) or ANG-(1-7) after precontraction with noradrenaline. HBOT rats were treated in a hyperbaric chamber with 100% O2(2 bar) 2 hours/day for 4 consecutive days. After intactness of endothelium was tested with acetylcholine, each ring was subjected to maximal contraction (using 60mM KCl + 0.1μM noradrenaline), and after washing/equilibration treated with either 1 μM ANG II (n[HBOT]=17; n[control]=16), 1 μM ANG II+1 μM ANG-(1-7) (n[HBOT]=14; n[control]=17), or noradrenaline 0.1 μM - for 5 minutes, after which 1 μM ANG-(1-7) was added and the ring tension read after 3 minutes (n[HBOT]=12; n[control]=17). The peak contraction force after ANG II and ANGII + ANG-(1-7) was expressed as percentage of maximal contraction, the effect of ANG-(1-7) addition was expressed as percentage of precontraction decrease after 3 minutes. RESULTS: Mean percentage of maximal contraction for ANGII was 21%±11 (HBOT) and 20%±9 (control) and was similar between groups (Mann-Whitney U test,P=1,000). The mean percentage for ANGII + ANG-(1-7) was 15% ±10 (HBOT) and 20%±9 (control); it tended to be decreased in the HBOT group, but without statistical significance (Mann-Whitney U test, P=0,054). There was a statistical significance when the mean percentage of maximal contraction of ANGII (HBOT) was compared to ANGII + ANG-(1-7) in the HBOT group (P=0,029(Mann-Whitney U)), without such a difference within the control group (P=0,953, t-test). Mean percentage of noradrenaline precontraction decrease with ANG(1-7) was 10%±9 (control) and 19%±11 (HBOT) - significantly different between groups (t-test, P=0,017). CONCLUSION: There was no change in reactivity to ANG II after HBOT. There may be an increase of reactivity to ANG-(1-7) after precontraction with noradrenaline, but since there was no significant effect of HBOT on the ANG II + ANG-(1-7) peak compared to control, at least at 1 μM concentrations, further studies are needed to conclusively interpret these results. Interestingly, there is a difference between the peak of ANGII in the HBOT group and ANGII + ANG-(1-7) in the HBOT group, whereas this difference was not present in the control group, suggesting an influence of HBOT on vascular reactivity.

Where applicable, experiments conform with Society ethical requirements