Abstract

Hydrogen sulfide ($\text{H}_2\text{S}$), a gaseous signaling molecule, is increasingly recognized as a critical modulator of smooth muscle function. This study investigates the effect of $\text{H}_2\text{S}$ on the spontaneous contractions of the rat jejunum, focusing specifically on the underlying role of various potassium ($\text{K}^+$) channels. Spontaneous contractions in the jejunum are driven by the rhythmic depolarization and repolarization of smooth muscle cells, a process fundamentally regulated by ion flux across the cell membrane. Using isolated segments of rat jejunum, we employed pharmacological agents to selectively block voltage-gated $\text{K}^+$ ($\text{K}_{\text{V}}$), calcium-activated $\text{K}^+$ ($\text{K}_{\text{Ca}}$), and inwardly rectifying $\text{K}^+$ ($\text{K}_{\text{ir}}$) channels while monitoring contractile activity in the presence and absence of $\text{H}_2\text{S}$. Our results demonstrate that $\text{H}_2\text{S}$ significantly reduces the amplitude and frequency of spontaneous jejunal contractions. This inhibitory effect was markedly attenuated by the blockade of $\text{K}_{\text{Ca}}$ channels, suggesting that $\text{H}_2\text{S}$ primarily acts by enhancing $\text{K}_{\text{Ca}}$ channel activity, leading to membrane hyperpolarization and reduced excitability. Blockade of $\text{K}_{\text{V}}$ and $\text{K}_{\text{ir}}$ channels had a lesser impact on the $\text{H}_2\text{S}$-mediated response. These findings highlight a crucial mechanism by which $\text{H}_2\text{S}$ regulates gastrointestinal motility, positioning $\text{K}_{\text{Ca}}$ channels as a key molecular target in the membrane for this gasotransmitter, with potential therapeutic implications for motility disorders.