Proceedings of The Physiological Society
University of Oxford (2011) Proc Physiol Soc 23, PC229
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 . Angotensin-(1-7) (ANG-(1-7))has been demonstrated to have dilating activity, in contrast to angiotensin II (ANG II) ; 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