Involvement of different K+ channel subtypes in hydrogen sulfide‐induced vasorelaxation of human internal mammary artery

Abstract Background Changes in K + channel expression/function are associated with disruption of vascular reactivity in several pathological conditions, including hypertension, diabetes, and atherosclerosis. Gasotransmitters achieve part of their effects in the organism by regulating ion channels, especially K + channels. Their involvement in hydrogen sulfide (H 2 S)‐mediated vasorelaxation is still unclear, and data about human vessels are limited. Objective To determine the role of K + channel subtypes in the vasorelaxant mechanism of H 2 S donor, sodium‐hydrosulfide (NaHS), on isolated human internal mammary artery (HIMA). Results NaHS (1 × 10 −6 –3 × 10 −3 mol/L) induced a concentration‐dependent relaxation of HIMA pre‐contracted by phenylephrine and high K + . Among K + channel blockers, iberiotoxin, glibenclamide, 4‐aminopyridine (4‐AP), and margatoxin significantly inhibited NaHS‐induced relaxation of phenylephrine‐contracted HIMA ( P 0.05). In the presence of nifedipine, NaHS induced partial relaxation of HIMA ( P < 0.01). Conclusion Our results demonstrated that H 2 S donor, NaHS, induced concentration‐dependent relaxation of isolated HIMA. Vasorelaxant mechanisms of H 2 S included direct or indirect opening of different K + channel subtypes, K ATP , BK Ca , SK Ca /IK Ca , and K V (subtype K V 1.3), in addition to NO pathway activation and interference with extracellular Ca 2+ influx.