Role of Potassium Channels in Leptin-Induced Uterine Relaxation in Late Pregnant Mice

Obesity is a significant risk factor for adverse reproductive outcomes, with leptin—an adipokine elevated in obesity—implicated in modulating uterine contractility through Maxi potassium (BK_Ca) channels. This study aimed to assess the role of Kz channels other than BK_Ca in leptin-induced uterine relaxation during late pregnancy in mice. Uterine strips from late pregnant Swiss albino mice were subjected to cumulative concentration–response curves to leptin (10{ ¹p to 10{ v M) in the presence of potassium channel blockers: 4-aminopyridine (4-AP, Kv), barium chloride (BaCl, , Kir2.1), and glibenclamide (K_ATP). Isometric contractions were recorded, and changes in maximal uterine inhibition (E_max) and potency (pD₂) were evaluated. Neither Kv nor Kir2.1 channel blockade using 4-aminopyridine (4-AP) and barium chloride (BaCl₂), respectively, significantly affected basal contractility or leptin-induced uterine relaxation. However, glibenclamide significantly reduced (p<0.05) the potency of leptin (pD2: 7.25 ± 0.26, n=6 vs. 8.58 ± 0.33, n=6) without altering E_max, suggesting a modulatory role of K_ATP channels in leptin responsiveness. While Kv and Kir2.1 channels appear to have minimal involvement, K_ATP channels may regulate the sensitivity of uterine smooth muscle to leptin. These findings offer insight into the ionic mechanisms underlying uterine quiescence and could inform therapeutic strategies for obesity-related pregnancy complications.