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  • We should also note that oxygen pressure of

    2019-11-16

    We should also note that oxygen pressure of Krebs solution bubbled with 95% O2+5% CO2 as we used in our study is reported to around 400 mmHg in several studies [48], [49], which is higher than normal arterial O2 pressure (80–100 mmHg). Although superoxide generation at elevated O2 tensions are noted to be higher, excessive superoxide generation might be unlikely in our experimental setting. It is safe to assume that NO was not being depleted by superoxide, since there was 85% relaxation response to ACh in WT group. On the other hand enhanced H2S production and decreased NO production is reported under lower O2 levels [50], [51]. Although we have used standard operating procedure with higher oxygen level than physiological conditions, in in vivo condition of lower O2 level, we may speculate to see augmented compensatory increase in H2S-induced relaxation in response to dysfunction of eNOS. However it is a very complex issue and not easy to make a prediction since the effect of oxygen level also differ from tissue to tissue. As a summary, while NaHS-induced relaxations were decreased, l-cysteine relaxations were increased by 77 of eNOS and it was on the opposite in eNOS overexpressed arteries. Our results suggest that the decrease in endogenous H2S-dependent relaxation accompanied with a compensatory increase in exogenous H2S-dependent relaxation to balance and maintain relaxation. Our results highlight the importance and compensatory protective role of H2S pathway in vascular pathologies. Slow releasing donors to supply safe elevation of H2S level instead of rapid donors may present a therapeutic potential in vascular pathologies where vasodilation is impaired.
    Conclusion Thus we suggest 1) a counter-regulatory role of NO on endogenous H2S dependent relaxation 2) a compensatory regulation of endogenous vs exogenous H2S-induced relaxations in mice carotid artery to maintain vascular relaxation.
    Acknowledgements This study was supported by TÜBITAK (The Scientific and Technological Research Council of Turkey) grant # 109s453 (GYA) allowing to joining COST action BM1005. The MC members (GYA and IF) thank COST action BM1005 for networking and the support by a STSM (EE).
    Introduction Legg-Calve-Perthes disease (LCPD) is an idiopathic osteonecrosis of the 77 femoral head epiphysis in children ≤15 years of age, with a maximum diagnosis at age between five and eight year.1, 2, 3 LCPD is usually unilateral and occurs five times more commonly in boys than in girls. The incidence of LCPD varies within certain ethnicities, partly depending on latitude., The incidence ranges from 0.4/100,000 to 29.0/100,000 children <15 years of age. The etiology and underlying pathophysiology of LCPD are still not completely understood, which makes it impossible to create prevention strategies or to identify individuals at risk. However, maternal smoking during pregnancy, small stature, skeletal retardation, and low birth weight seems to be the key pathogenetic causes of LCPD., Generally, it seems LCPD is usually not caused by genetic factors, but there are some cases where LCPD affects multiple family members. In addition, in a few familial cases an autosomal dominant inheritance has been reported., This complexity makes it very difficult to predict whether or not an individual will inherit LCPD. Understanding genetic basis of LCPD is yet to be achieved, although this field has been increasing in recent years. Some studies have examined the relationship between genetic diversity and LCPD susceptibility. Evidence is growing that genetic variations in the COL2A1,, eNOS, TLR4, IL-6, α, FV, FII, and MTHFR genes to be responsible on the likelihood of developing LCPD. The eNOS (MIM: 163729; GenBank ID: 4846) gene is located on chromosome 7q35-36, comprises 26 exons, and spanning 21 kb. The eNOS gene is one of the factors that regulate the expression of the endotheliocyte gene. Three polymorphisms of the eNOS gene have been identified, including a T786C (rs2070744) polymorphism in the promoter region, a G894T (rs1799983) polymorphism in exon 7 and a variable number of tandem 4a4b repeats (rs61722009) in intron 4., Studies results showed that each polymorphism can influence the expression or functional activity of eNOS enzyme.