Rat thoracic aorta and mesenteric artery show a multiphasic contraction‐relaxation‐contraction response to sodium sulfide and sodium hydrosulfide

Abstract

Hydrogen sulfide (H2S) is now a recognized gas signaling molecule in the cardiovascular system, joining nitric oxide and carbon monoxide. H2S has been shown to cause relaxation in rat thoracic aorta (TA) and mesenteric artery (MA), as well as multiphasic responses in pulmonary artery and other vertebrate vessels. While relaxation occurs shortly after H2S addition, multiphasic responses require more time to observe. Therefore in this study, we hypothesized that TA and MA would show a multiphasic response to H2S if time were allowed for completion. TA and MA were dissected from Fisher 344 x Brown Norway rats. TA was sectioned into rings and run on a wire myograph, and MA was run on a pressure arteriograph. H2S was added via the donors sodium sulfide (Na2S) or sodium hydrosulfide (NaHS) after preconstriction with phenylephrine. Both TA and MA showed a triphasic contraction‐relaxation‐contraction response using either H2S donor. The first contraction was quick and small in magnitude. A sustained relaxation followed, after which a second sustained contraction much larger in magnitude than the first occurred. Overall the triphasic response was complete in 15‐30 min. These data show that H2S signaling in mammalian vessels is more complex than a monophasic relaxation, regardless of the H2S donor, and therefore the entire mulitphasic response to H2S should be considered when investigating potential H2S signaling mechanisms.