Tectorigenin induces vasorelaxation in porcine coronary arteries through activation of Kv channels and oestrogen receptor modulation.

Ischaemic heart disease remains a leading cause of mortality worldwide, highlighting the need for new agents that protect vascular function. Tectorigenin, a plant-derived isoflavone, is known for its anti-inflammatory and antioxidant properties, but its direct effects on vascular tone have not been clearly explored. This study investigated the vasorelaxant actions of tectorigenin in endothelium-denuded porcine coronary arteries and examined the mechanisms involved. Using isolated artery rings pre-contracted with a thromboxane A₂ analogue, we found that tectorigenin induced concentration-dependent relaxation with an EC₅₀ of approximately 11 µM. Pharmacological inhibition experiments revealed that relaxation at 10-30 µM was significantly reduced by oestrogen receptor antagonists and by 4-aminopyridine, a blocker of voltage-gated potassium channels, and was completely abolished under high-potassium conditions. In contrast, inhibitors targeting neural conduction, nitric oxide synthase, cyclic nucleotide pathways, and other potassium channels had no significant impact. Immunohistochemistry and qPCR analyses indicated predominant ERα expression in the coronary arteries. These findings are consistent with contributions from oestrogen receptors (with ERα predominance) and 4-AP-sensitive Kv channels to the relaxant response; a direct ER-Kv coupling was not established in this ex vivo model. This is the first study to characterise the vascular pharmacology of tectorigenin in a large-animal coronary model. Further in vivo investigations are warranted to assess its potential in managing cardiovascular diseases.