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First published online August 3, 2006
Journal of Experimental Biology 209, 3234-3240 (2006)
Published by The Company of Biologists 2006
doi: 10.1242/jeb.02376

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Hydrogen sulfide mediates hypoxia-induced relaxation of trout urinary bladder smooth muscle

Ryan A. Dombkowski^1,2, Meredith M. Doellman², Sally K. Head² and Kenneth R. Olson^1,2,*

¹ South Bend Center for Medical Education, Indiana University School of Medicine, University of Notre Dame, Notre Dame, IN 46556, USA
² Department of Biological Sciences, University of Notre Dame, Notre Dame, IN 46556, USA

^* Author for correspondence (e-mail: kolson{at}nd.edu)

Accepted 8 June 2006

Hydrogen sulfide (H₂S) is a recently identified gasotransmitter that may mediate hypoxic responses in vascular smooth muscle. H₂S also appears to be a signaling molecule in mammalian non-vascular smooth muscle, but its existence and function in non-mammalian non-vascular smooth muscle have not been examined. In the present study we examined H₂S production and its physiological effects in urinary bladder from steelhead and rainbow trout (Oncorhynchus mykiss) and evaluated the relationship between H₂S and hypoxia. H₂S was produced by trout bladders, and its production was sensitive to inhibitors of cystathionine ß-synthase and cystathionine -lyase. H₂S produced a dose-dependent relaxation in unstimulated and carbachol pre-contracted bladders and inhibited spontaneous contractions. Bladders pre-contracted with 80 mmol l^-1 KCl were less sensitive to H₂S than bladders contracted with either 80 mmol l^-1 KC₂H₃O₂ (KAc) or carbachol, suggesting that some of the H₂S effects are mediated through an ion channel. However, H₂S relaxation of bladders was not affected by the potassium channel inhibitors, apamin, charybdotoxin, 4-aminopyridine, and glybenclamide, or by chloride channel/exchange inhibitors 4,4'-Diisothiocyanatostilbene-2,2'-disulfonic acid disodium salt, tamoxifen and glybenclamide, or by the presence or absence of extracellular HCO₃^-. Inhibitors of neuronal mechanisms, tetrodotoxin, strychnine and N-vanillylnonanamide were likewise ineffective. Hypoxia (aeration with N₂) also relaxed bladders, was competitive with H₂S for relaxation, and it was equally sensitive to KCl, and unaffected by neuronal blockade or the presence of extracellular HCO₃^-. Inhibitors of H₂S synthesis also inhibited hypoxic relaxation. These experiments suggest that H₂S is a phylogenetically ancient gasotransmitter in non-mammalian non-vascular smooth muscle and that it serves as an oxygen sensor/transducer, mediating the effects of hypoxia.

Key words: H₂S, hypoxia, smooth muscle, urinary bladder, trout

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