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Rat thoracic aorta and mesenteric artery show a multiphasic contraction‐relaxation‐contraction response to sodium sulfide and sodium hydrosulfide
Author(s) -
Predmore Benjamin Lee,
Whidden Melissa A.,
Erdos Benedek,
Tumer Nihal,
Julian David
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.628.11
Subject(s) - sodium hydrosulfide , contraction (grammar) , myograph , medicine , phenylephrine , chemistry , sodium , cardiology , aorta , anesthesia , endocrinology , hydrogen sulfide , blood pressure , sulfur , organic chemistry
Hydrogen sulfide (H 2 S) is now a recognized gas signaling molecule in the cardiovascular system, joining nitric oxide and carbon monoxide. H 2 S 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 H 2 S addition, multiphasic responses require more time to observe. Therefore in this study, we hypothesized that TA and MA would show a multiphasic response to H 2 S 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. H 2 S was added via the donors sodium sulfide (Na 2 S) or sodium hydrosulfide (NaHS) after preconstriction with phenylephrine. Both TA and MA showed a triphasic contraction‐relaxation‐contraction response using either H 2 S 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 H 2 S signaling in mammalian vessels is more complex than a monophasic relaxation, regardless of the H 2 S donor, and therefore the entire mulitphasic response to H 2 S should be considered when investigating potential H 2 S signaling mechanisms.