Telmisartan ameliorates vascular endothelial dysfunction in coronary slow flow phenomenon (CSFP)

Coronary slow flow phenomenon (CSFP) is a coronary microvascular disorder with an increasing morbidity, and currently, available therapies are of limited clinical value for its cure. Hence, it is urgent to find a novel approach to CSFP treatment. Several studies show that endothelial dysfunction plays a critical role in the aetiology of CSFP. Telmisartan (TMST) is a clinically available anti‐hypertensive medicine and has shown its potential properties for improving vascular endothelial function. Thus, we aimed to investigate the effect of TMST on endothelial dysfunction in CSFP, Endothelial‐dependent flow‐mediated vasodilation, serum levels of nitric oxide, adiponectin, and endothelin‐1 were surveyed before and after 3 months of TMST treatment. And the percentages of vasodilator response to acetylcholine (Ach) were detected after 12 weeks of TMST treatment. Compare with pretreatment, flow‐mediated vasodilation, nitric oxide, and adiponectin were substantially improved after TMST treatment; meanwhile, endothelin‐1 was decreased in the TMST group (all P < .01). Compared with the model group, the vasodilator response to Ach was enormously increased after TMST intervention. Additionally, administration of SU11274 or GW9662 would partially reverse the protective effects of TMST on accumulative concentration‐vasodilator responses to Ach (P < .01). We demonstrated that administration of TMST could remarkably increase the mRNA and/or protein levels of hepatocyte growth factor, mesenchymal‐epithelial transition factor, peroxisome proliferation‐activated receptor γ, whereas dramatically diminish mRNA and/or protein levels of p‐JNK1/2, mitogen‐activated protein kinase, and nuclear factor kappa B (P < .05). Our results thus implicate that TMST ameliorates endothelial dysfunction in CSFP. It is suggested that TSMF may play an important role in the medication of CSFP.