Hydrogen sulfide as a mediator of human corpus cavernosum smooth-muscle relaxation

Bianca, Roberta d’Emmanuele di Villa; Sorrentino, Raffaella; Maffia, Pasquale; Mirone, Vincenzo; Imbimbo, Ciro; Fusco, Ferdinando; Palma, Raffaele De; Ignarro, Louis J.; Cirino, Giuseppe

doi:10.1073/pnas.0807974105

Cited by 186 publications

(136 citation statements)

References 39 publications

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“…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. 2,5,6,7,23,24 Taken together, we proposed that the effect of H 2 S on human and rat bladder smooth muscle tone might play various roles, depending on different pretreatments. 20,21 In our study, exogenous and endogenous H 2 S relaxed smooth muscle that was pre-contracted with acetylcholine chloride.…”

Section: Discussionmentioning

confidence: 99%

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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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Section: Discussionmentioning

confidence: 99%

“…[4][5][6][7] Bucci et al 8 even noted that H 2 S was involved in testosterone vascular effects, which made H 2 S more attractive for urological researchers. Our previous study had also revealed the expression and characterisation of H 2 S in human prostatic tissue and cell lines.…”

Section: Introductionmentioning

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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“…[29][30][31] H 2 S inhibits oxidative stress, promotes stimulation of adenosine triphosphate-senstive potassium (K ATP ) channels, and relaxation and vasodilation in vascular smooth muscle cells and of the human corpus cavernous smooth muscle. 27,[29][30][31][32][33][34] Genetic deletion of the CSE enzyme in mice markedly reduces H 2 S levels in the serum, heart, aorta, and other tissues, and mice lacking CSE display pronounced hypertension and diminished endothelium dependent vasorelaxation. 27 Furthermore, ApoE knockout mice treated with a H 2 S donor showed reduced atherosclerotic plaque size compared to controls.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Sleep Apnea and Insomnia on Blood Levels of Leptin, Insulin Resistance, IP-10, and Hydrogen Sulfide in Type 2 Diabetic Patients

Jain

Kahlon²,

Morehead³

et al. 2012

Metabolic Syndrome and Related Disorders

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Introduction: Sleep deficits associated with sleep apnea and insomnia increase the risk of vascular inflammation and insulin resistance. This study examined the hypothesis that inflammation markers are higher in those diabetic patients who experience sleep deficits compared with those without any history of a sleep disorder. Methods: Fasting blood was obtained after written informed consent, and sleep disorder histories were obtained from type 2 diabetic patients (n = 81) attending clinics of the Louisiana State University Health Sciences Center.Results: There was a significant correlation between body weight and leptin, and leptin in turn was significantly correlated with 10-kDa interferon-g-induced protein (IP-10) levels and insulin resistance in type 2 diabetic patients. Fasting blood levels of leptin, IP-10, and insulin resistance were significantly elevated in patients with sleep deficits compared with diabetics with normal sleep patterns. There were no differences in glycosylated hemoglobin (HbA1c) or fasting glucose in patients with sleep deficits compared with those with normal sleep patterns. Sleep deficits increase circulating levels of leptin, IP-10, and insulin resistance compared to levels seen in patients with diabetes who reported no difficulty with sleep. Patients with sleep apnea had significantly lower hydrogen sulfide (H 2 S) levels compared with patients with normal sleep patterns or patients with insomnia. Low levels of circulating H 2 S could contribute to higher vascular inflammation in patients with sleep apnea. Conclusions: These results suggest that sleep apnea is associated with a decrease in circulating H 2 S and sleep disorders increase the risk of inflammation and insulin resistance, which can contribute to the increased risk of vascular disease in subjects with type 2 diabetes.

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“…H 2 S also relaxes human corpus cavernosum and urinary bladder smooth muscle (24,45). 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).…”

Section: Other Tissuesmentioning

confidence: 99%

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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Hydrogen sulfide as a mediator of human corpus cavernosum smooth-muscle relaxation

Cited by 186 publications

References 39 publications

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

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

The Effect of Sleep Apnea and Insomnia on Blood Levels of Leptin, Insulin Resistance, IP-10, and Hydrogen Sulfide in Type 2 Diabetic Patients

Hydrogen sulfide as an oxygen sensor

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