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

Dombkowski, Ryan A.; Doellman, Meredith M.; Head, Sally K.; Olson, Kenneth R.

doi:10.1242/jeb.02376

Cited by 62 publications

(38 citation statements)

References 28 publications

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“…Addition of exogenous cysteine, which presumably enhances or sustains H 2 S production, augments hypoxic relaxation of trout urinary bladder (31) and salmon intestine (32). Consistent with findings in other tissues, inhibitors of H 2 S biosynthesis inhibit hypoxic relaxation of rainbow trout urinary bladder (31) and rainbow trout and Coho salmon intestine (32).…”

Section: Other Tissuessupporting

confidence: 56%

“…Hypoxia and H 2 S also relax nonvascular smooth muscle of fish urinary bladder and the gastrointestinal tract, both of these stimuli produce a unique and transient increase in spontaneous contraction frequency and amplitude before the onset of the inhibitory effects (31,32). H 2 S also relaxes human corpus cavernosum and urinary bladder smooth muscle (24,45).…”

Section: Other Tissuesmentioning

confidence: 99%

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Hydrogen sulfide as an oxygen sensor

Olson

2013

Clinical Chemistry and Laboratory Medicine

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Significance: Although oxygen (O 2 )-sensing cells and tissues have been known for decades, the identity of the O 2 -sensing mechanism has remained elusive. Evidence is accumulating that O 2 -dependent metabolism of hydrogen sulfide (H 2 S) is this enigmatic O 2 sensor. Recent Advances: The elucidation of biochemical pathways involved in H 2 S synthesis and metabolism have shown that reciprocal H 2 S/O 2 interactions have been inexorably linked throughout eukaryotic evolution; there are multiple foci by which O 2 controls H 2 S inactivation, and the effects of H 2 S on downstream signaling events are consistent with those activated by hypoxia. H 2 S-mediated O 2 sensing has been demonstrated in a variety of O 2 -sensing tissues in vertebrate cardiovascular and respiratory systems, including smooth muscle in systemic and respiratory blood vessels and airways, carotid body, adrenal medulla, and other peripheral as well as central chemoreceptors. Critical Issues: Information is now needed on the intracellular location and stoichometry of these signaling processes and how and which downstream effectors are activated by H 2 S and its metabolites. Future Directions: Development of specific inhibitors of H 2 S metabolism and effector activation as well as cellular organelle-targeted compounds that release H 2 S in a timeor environmentally controlled way will not only enhance our understanding of this signaling process but also provide direction for future therapeutic applications. Antioxid. Redox Signal. 22, 377-397.

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Section: Other Tissuessupporting

confidence: 56%

Section: Other Tissuesmentioning

confidence: 99%

Hydrogen sulfide as an oxygen sensor

Olson

2013

Clinical Chemistry and Laboratory Medicine

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“…[20][21][22] We observed in the midst of H 2 S, the relaxation of smooth muscle precontracted with acetylcholine chloride. Streng et al 20 investigated the transient receptor potential vanilloid receptor 1 and showed that it might be involved in the contraction induced by NaHS when rat bladder strips were electrically stimulated.…”

Section: Discussionmentioning

confidence: 80%

“…Patacchini et al 21 reported Expression and function of hydrogen sulphide in human and rat bladder JW Gai et al 694 that intravesical NaHS instillation increased protamine sulphate pretreated rat bladder pressure. Dombkowski et al 22 explored the H 2 S effects on trout bladder smooth muscle and suggested that H 2 S could produce a dose-dependent relaxation in unstimulated and carbachol pre-contracted bladders and inhibit spontaneous contractions. KCl, adrenergic and cholinergic agonists would usually be chosen to precontract smooth muscle in not only LUT but also cardiovascular vessels, gastrointestinal tract, and corpus cavernosum tissues.…”

Section: Discussionmentioning

confidence: 99%

Further evidence of endogenous hydrogen sulphide as a mediator of relaxation in human and rat bladder

Gai

Wahafu²,

Guo³

et al. 2013

Asian J Androl

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We investigated the expression of hydrogen sulphide (H 2 S) in human and rat lower urinary tract (including bladder, prostate and urethra) tissues, and we sought to determine whether H 2 S induces relaxation of human and Sprague-Dawley (SD) rat bladder strips. Human normal lower urinary tract tissue was obtained for the evaluation of endogenous H 2 S productivity using a sulphide-sensitive electrode and for the analysis of the expression levels of all three synthases of endogenous H 2 S, cystathionine b-synthase (CBS), cystathionine c lyase (CSE) and 3-mercaptopyruvate sulphur transferase (MPST, as known as 3-MST) by Western blot assay. CBS, CSE and MPST were located in human sample slides by immunohistochemistry. Human and male adult SD rat bladder strips were tested for H 2 S function with a transducer and recorded. All experiments were repeated six times. The endogenous H 2 S productivity and the H 2 S synthases had various distributions in the human and rat lower urinary tract tissues and were located in both epithelial and stromal sections. L-cysteine (L-Cys, a substrate of CBS, CSE and MPST) elicited relaxation in a dose-dependent manner on human bladder strips pre-contracted by acetylcholine chloride. This effect could be diminished by the ATP-sensitive potassium ion (K ATP ) channel blocker glibenclamide (GLB), the CSE inhibitor DL-propargylglycine (PPG) and the CBS inhibitor hydroxylamine (HA). H 2 S and its three synthases were present in the human and rat lower urinary tract tissues and relaxed human and rat bladder strips, which implied that endogenous H 2 S might play a role in physiological function and pathological disorders of the lower urinary tract symptoms (LUTS) or overactive bladder (OAB).

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“…Therefore, assuming that H 2 S is the vasoactive sulfide moiety, anoxic turtles did not display hemodynamic responses to NaHS despite the fact they experienced a greater exogenous H 2 S exposure than normoxic turtles and the amount of H 2 S produced upon infusion of 30 mol/kg NaHS exceeded the estimated circulating plasma H 2 S levels. However, the local intracellular concentration of H 2 S produced endogenously by vascular smooth muscle (12,26,48,83,84) may have been higher. If the activation of the signaling pathway of H 2 S-mediated vasoconstriction is maximal during anoxia, it would be expected that R sys and/or P sys should fall, and/or G sys increase, in response to antagonists of endogenous H 2 S production.…”

Section: Does H 2 S Contribute To the Increased R Sys Of Anoxic Turtles?mentioning

confidence: 99%

Vasoactivity of hydrogen sulfide in normoxic and anoxic turtles (Trachemys scripta)

Stecyk

Skovgaard

Nilsson

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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of hydrogen sulfide in normoxic and anoxic turtles (Trachemys scripta). Am J Physiol Regul Integr Comp Physiol 298: R1225-R1239, 2010. First published February 17, 2010 doi:10.1152/ajpregu.00521.2009.-Systemic vascular resistance (Rsys) of freshwater turtles increases substantially during anoxia, but the underlying mechanisms are not fully understood. We investigated whether hydrogen sulfide (H2S), an endogenously produced metabolite believed to be an O 2 sensor/ transducer of vasomotor tone, contributes to the increased R sys of anoxic red-eared slider turtles (Trachemys scripta). Vascular infusion of the H 2S donor NaHS in anesthetized turtles at 21°C and fully recovered normoxic turtles at 5°C and 21°C revealed H 2S to be a potent vasoconstrictor of the systemic circulation. Likewise, wire myography of isolated turtle mesenteric and pulmonary arteries demonstrated H 2S to mediate an anoxia-induced constriction. Intriguingly, however, NaHS did not exert vasoconstrictory effects during anoxia (6 h at 21°C; 14 days at 5°C) when plasma H 2S concentration, estimated from the colorimetric measurement of plasma acid-labile sulfide concentration, likely increased by ϳ3-and 4-fold during anoxia at 21°C, and 5°C, respectively. Yet, blockade of endogenous H 2S production by DL-propargylglycine or hydroxylamine (0.44 mmol/kg) partially reversed the decreased systemic conductance (G sys) exhibited by 5°C anoxic turtles. These findings suggest that the signal transduction pathway of H 2S-mediated vasoactivity is either maximally activated in the systemic circulation of anoxic turtles and/or that it is oxygen dependent. red-eared slider; anoxia; temperature; cardiovascular; systemic resistance; pulmonary resistance; blood pressure; heart NORTH AMERICAN FRESHWATER turtles of the genera Trachemys, Chrysemys, and Chelydra exhibit a remarkable ability to survive a prolonged lack of oxygen (anoxia). At high temperatures (20 -25°C), these turtles successfully recover after 24 h of anoxia, but they can survive weeks to months without oxygen at the low temperatures, at which these animals overwinter (3-5°C) (57, 71). The exceptional anoxia tolerance is achieved through a profound reduction of whole animal metabolic rate, which slows metabolic fuel use and the rate of waste accumulation (21, 30) and the ability to use bone and shell as buffers to ameliorate the catastrophic acidosis that otherwise would accompany the sustained anaerobic metabolism (29,53).The large reduction in metabolism is attended by a pronounced lowering of cardiovascular performance during anoxia, where heart rate (f H ) and systemic blood flow (Q sys ) are drastically reduced and where pulmonary blood flow (Q pul ) virtually ceases (16,23,25,(65)(66)(67). While systemic blood pressure (P sys ) also decreases during anoxia, the reduction in Q sys is considerably larger, indicating a substantial (3-to 5-fold) increase in systemic peripheral resistance (R sys ). At high temperatures, the rise in R sys is largely due to increased ␣-adrenergic tone (54, 65), but ...

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

Abstract: Inhibitors of H 2 S synthesis also inhibited hypoxic relaxation. These experiments suggest that H 2 S is a phylogenetically ancient gasotransmitter in nonmammalian non-vascular smooth muscle and that it serves as an oxygen sensor/transducer, mediating the effects of hypoxia.

Cited by 62 publications

References 28 publications

Hydrogen sulfide as an oxygen sensor

Hydrogen sulfide as an oxygen sensor

Further evidence of endogenous hydrogen sulphide as a mediator of relaxation in human and rat bladder

Vasoactivity of hydrogen sulfide in normoxic and anoxic turtles (Trachemys scripta)

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