The vasodilator effect of apigenin (API) was demonstrated in a number of vascular beds. We aimed to characterize the vasospasmolytic and electrophysiological effects of apigenin (API) in intrarenal arteries (IRAs). The vascular tone of male rat isolated IRAs was recorded with a myograph. Transmembrane Cl ⁻ currents through Ca ²⁺ -activated Cl ⁻ channels (CaCCs), K ⁺ currents through voltage-gated K ⁺ (Kv) channels and inwardly rectifier K ⁺ (Kir) channels were recorded with patch clamp in the freshly isolated arterial smooth muscle cells (ASMCs). Preincubation with API (10-100 μM) concentration-dependently depressed the contractions induced by KCl, 9,11-dideoxy-9α,11α-methanoepoxy prostaglandin F _2α (U46619), phenylephrine and vasopressin without significant preference and the IC ₅₀ values were 13.27-26.26 μM. Acute application of API elicited instant relaxations in the IRAs precontracted with these vasoconstrictors and the RC ₅₀ values were 5.80-24.33 μM. API relaxation was attenuated by chloride deprivation, CaCC blockers, Kv blocker and nitric oxide synthase inhibitor, but not by Kir blocker and cyclooxygenase inhibitor. At 10-100 μM, API depressed CaCC currents and Kir currents while enhanced Kv currents of IRA ASMCs. The present results demonstrate that API counteracts various vasoconstrictors noncompetitively and nonspecifically and suggest that modulation of CaCCs, Kv and Kir channels of IRA ASMCs is involved in its vasospasmolytic effects.

Cerebrovascular disease is a prevalent condition among the elderly, with its incidence steadily rising. The basilar artery is a critical cerebral vessel that supplies the pons, cerebellum, posterior brain regions, and inner ear. Potassium (K+) channel activity plays a significant role in determining vascular tone by regulating the cell membrane potential. Activation of inward rectifying K+ (Kir) channels, like other K+ channels, leads to cell membrane hyperpolarization and vasodilation. In this study, freshly isolated smooth muscle cells from the basilar artery were used to record Kir currents via the whole-cell patch clamp technique. The effects of 100 µmol/L BaCl2, a Kir channel inhibitor, and 10 µmol/L sodium nitroprusside (SNP), a nitro vasodilator, on Kir channel currents were investigated. The results demonstrated that BaCl2 inhibited Kir channel currents in basilar artery smooth muscle cells, whereas SNP enhanced these currents. This protocol provides a comprehensive guide for preparing freshly isolated arterial smooth muscle cells and recording Kir channel currents using the patch clamp technique, offering a valuable resource for researchers seeking to master this method.

Cerebrovascular disease is a prevalent condition among the elderly, with its incidence steadily rising. The basilar artery is a critical cerebral vessel that supplies the pons, cerebellum, posterior brain regions, and inner ear. Potassium (K+) channel activity plays a significant role in determining vascular tone by regulating the cell membrane potential. Activation of inward rectifying K+ (Kir) channels, like other K+ channels, leads to cell membrane hyperpolarization and vasodilation. In this study, freshly isolated smooth muscle cells from the basilar artery were used to record Kir currents via the whole-cell patch clamp technique. The effects of 100 µmol/L BaCl2, a Kir channel inhibitor, and 10 µmol/L sodium nitroprusside (SNP), a nitro vasodilator, on Kir channel currents were investigated. The results demonstrated that BaCl2 inhibited Kir channel currents in basilar artery smooth muscle cells, whereas SNP enhanced these currents. This protocol provides a comprehensive guide for preparing freshly isolated arterial smooth muscle cells and recording Kir channel currents using the patch clamp technique, offering a valuable resource for researchers seeking to master this method.