Division of Pharmacology and Toxicology, ICAR-Indian Veterinary Research Institute, Izatnagar-243 122, Bareilly, Uttar Pradesh, India
*Corresponding author Email: tusingh80@gmail.com
Online published on 11 August, 2021.
This study evaluated the dilatory potential of biochanin-A in the pulmonary vasculature of rat and further, to evaluate signaling mechanisms. Experiments were conducted on the organ bath system and tension generated by the pulmonary artery of rats was recorded with the help of data acquisition system. Biochanin-A (10-7-10-4 M) showed concentrations-dependent vasorelaxation in both endothelium-intact and -denuded rat isolated pulmonary artery and this relaxation was not different with each other. Further, biochanin-A-induced relaxation was not influenced by the LNAME and indomethacin. Rat pulmonary arterial rings precontracted with the high potassium depolarizing solution showed a significant reduction in vasorelaxation. Further, Kv channel blocker, 4-AP showed a significant reduction in the vascular relaxation. Nevertheless, KATP channel blocker, glibenclamide, and Kir channel blocker, BaCl2, did not influence the biochanin-A-induced vasorelaxation. TEA did not reduce the relaxation, however, at one concentration, it influenced the relaxation response. A significant reduction in relaxation was observed in the presence of sGC inhibitor ODQ. Further, protein kinase blocker H89, estrogen receptor antagonist ICI182780 and TRPV4 channel blocker HC067047 did not reduce the relaxation induced by biochanin-A in rat pulmonary artery. In conclusion, rat isolated pulmonary artery showed vasorelaxation due to biochanin-A may be mediated through KV channels and sGC pathways.
Biochanin-A, Relaxation, Pulmonary artery, Sgc, Rat