Abstract:
This research explores the effects of Qibaipingfei (QBPF) capsules on pulmonary vascular relaxation in vitro
and the relationship of the ATP-sensitive K+ (KATP) channel and nitric oxide (NO) pathway. Vasodilator effects of QBPF (0.125-2 g/kg) on rat pulmonary artery rings were observed using a multi-wire myograph system. The maximum relaxation (Emax) of QBPF was detected following treatment involving endothelial denudation, Nω-nitro-L-arginine methyl ester (L-NAME), 1H-[1,2,4] oxadiazolo[4,3-α]quinoxalin-1-one (ODQ), or glyburide (GLYB). Furthermore, rat models of phlegm and blood stasis syndrome combined with chronic obstructive pulmonary disease (COPD) were established using compound factors. KIR6.1 and SUR2B protein expression was analyzed by western blotting. After 9,11-dideoxy-11α,9α-epoxy-methanoprostaglandinF2α (U46619) was used to pre-constrict endothelium-intact pulmonary artery rings, QBPF induced the effects of concentration-dependent relaxation at a concentration for 50% of maximal effect (EC50) of 0.56 g/L and Emax of 84.30% ± 6.27%. After the endothelium was denuded, the vasodilator effects reduced significantly (P<0.01). QBPF-induced relaxation was inhibited by L-NAME, ODQ, and GLYB (P<0.01). The vasodilator effect was also attenuated in the model group (Emax=62.63%±10.02, EC50 = 0.72 g/L, P<0.01). In comparison with expression in the control group, SUR2B protein expression was down-regulated in the model group (P<0.01) but no significant difference was detected in KIR6.1 protein expression between the groups (P>0.05). QBPF and nicorandil (Nic) treatment up-regulated SUR2B KATP channel expression (P<0.05). QBPF induces endothelial-dependent relaxation in pulmonary artery rings in vitro, through a mechanism that potentially activates the KATP channel in pulmonary vascular smooth muscles via the NO-cyclic GMP (cGMP)-dependent pathway.
