A modified aortic multiple-ring preparation for functional studies

Calderone, Vincenzo; Martinotti, Enrica; Scatizzi, R; Pellegrini, Antonio; Breschi, Maria Cristina

doi:10.1016/1056-8719(96)00023-8

Cited by 19 publications

(8 citation statements)

References 28 publications

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“…Hosoki et al (13) used helical tissue strips of the aorta from Wistar rats, and we used aortic rings from Sprague-Dawley rats. The tissue damage of helical strips is certainly greater than that of ring preparations (4). This may also explain why, in the study by Hosoki et al (13), the vasorelaxant potency of NaHS was much greater in portal vein rings than in aorta strips.…”

mentioning

confidence: 60%

H₂S-induced vasorelaxation and underlying cellular and molecular mechanisms

Zhao

Wang

2002

American Journal of Physiology-Heart and Circulatory Physiology

462

385

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Zhao, Weimin, and Rui Wang. H2S-induced vasorelaxation and underlying cellular and molecular mechanisms. Am J Physiol Heart Circ Physiol 283: H474-H480, 2002. First published April 18, 2002 10.1152/ajpheart.00013. 2002 is endogenously generated in vascular smooth muscle cells. The signal transduction pathways involved in the vascular effects of H2S have been unclear and were investigated in the present study. H 2S induced a concentration-dependent relaxation of rat aortic tissues that was not affected by vascular denervation. The vasorelaxant potency of H2S was attenuated by the removal of the endothelium. Similarly, the blockade of nitric oxide synthase or the coapplication of the Ca 2ϩ -dependent K ϩ channel blockers apamin and charybdotoxin reduced the H2S-induced relaxation of the endothelium-intact aortic tissues. Sodium nitroprusside (SNP)-induced relaxation was completely abolished by either 1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one (ODQ) or NS-2028, two soluble guanylate cyclase inhibitors. Instead of inhibition, ODQ and NS-2028 potentiated the H2S-induced vasorelaxation, which was suppressed by superoxide dismutase. The vasorelaxant effect of H2S was also significantly attenuated when Ca 2ϩ -free bath solution was used. Finally, pretreatment of aortic tissues with H2S reduced the relaxant response of vascular tissues to SNP. Our results demonstrate that the vascular effect of H2S is partially mediated by a functional endothelium and dependent on the extracellular calcium entry but independent of the activation of the cGMP pathway. aorta; guanosine 3Ј,5Ј-cyclic monophosphate; endothelium H 2 S HAS BEEN GENERALLY CONSIDERED as a toxic gas found in the contaminated environmental atmosphere. Its major toxic effects are the toxication of central nervous system and the inhibition of the respiratory system (2, 10, 28). H 2 S can also be produced endogenously from L-cysteine by cystathionine ␤-synthase (CBS) and/or cystathionine ␥-lyase (CSE) (23,24). The expression of these enzymes has been detected in various tissues (13). Our recent study (31) demonstrated that CSE was expressed in the rat aorta, tail artery, mesenteric artery, and pulmonary artery, whereas the expression of CBS was not detectable. Under physiological conditions, tissue content of H 2 S in the brain has been determined to be between 50 and 160 M (1). The endogenous production of H 2 S from rat vascular tissues has also been demonstrated in our previous study (31). With the use of a modified sulfide electrode method, the H 2 S concentration of rat serum was determined to be ϳ46 M (31). These observations speak for the potential physiological functions of H 2 S in the cardiovascular system.The relaxant effects of exogenously applied H 2 S on intestinal and vascular smooth muscles have been reported (13). In both the aorta and portal vein of rats, H 2 S induced a dose-dependent relaxation, but other thiol-containing endogenous substances such as cysteine and glutathione did not have any vasorelaxant effect (13). More importantly, we found ...

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mentioning

confidence: 60%

H₂S-induced vasorelaxation and underlying cellular and molecular mechanisms

Zhao

Wang

2002

American Journal of Physiology-Heart and Circulatory Physiology

462

385

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“…Finally, concentrations of Ͻ30 M H 2 S cause no apparent disturbance in oxidative phosphorylation because of the rapid oxidation of H 2 S in mitochondria (Guidotti, 1996). Recent data demonstrated that physiologic plasma H 2 S concentrations in rats are Ϸ46 M (Calderone at al., 1996). In the present study, the plasma concentrations of H 2 S ranged from 30 to 55 M, unlikely making it a central toxic effect of the gas.…”

Section: Discussionmentioning

confidence: 99%

Evidence That Hydrogen Sulfide Exerts Antinociceptive Effects in the Gastrointestinal Tract by Activating K_ATP Channels

Distrutti

Sediari²,

Mencarelli³

et al. 2005

J Pharmacol Exp Ther

246

212

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Hydrogen sulfide (H 2 S) functions as a neuromodulator, but whether it modulates visceral perception and pain is unknown. Cystathionine ␤-synthase (CBS) and cystathionine-␥-lyase (CSE) mediate enzymatic generation of H 2 S in mammalian cells. Here we have investigated the role of H 2 S in modulating nociception to colorectal distension, a model that mimics some features of the irritable bowel syndrome. Four graded (0.4 -1.6 ml of water) colorectal distensions (CRDs) were produced in conscious rats (healthy and postcolitic), and rectal nociception was assessed by measuring the behavioral response during CRD. Healthy rats were administered with sodium hydrogen sulfide (NaHS) (as a source of H 2 S), L-cysteine, or vehicle. In a second model, we investigated nociception to CRD in rats recovering from a chemically induced acute colitis. We found that CBS and CSE are expressed in the colon and spinal cord.Treating rats with NaHS resulted in a dose-dependent attenuation of CRD-induced nociception with the maximal effect at 60 mol/kg (p Ͻ 0.05). Administration of L-cysteine, a CSE/CBS substrate, reduced rectal sensitivity to CRD (p Ͻ 0.05). NaHSinduced antinociception was reversed by glibenclamide, a ATP-sensitive K ϩ (K ATP ) channel inhibitor, and N -nitro-L-arginine methyl ester hydrochloride (L-NAME), a nitric-oxide (NO) synthase inhibitor. The antinociceptive effect of NaHS was maintained during the resolution of colon inflammation induced by intrarectal administration of a chemical irritant. In summary, these data show that H 2 S inhibits nociception induced by CRD in both healthy and postcolitic rats. This effect is mediated by K ATP channels and NO. H 2 S-releasing drugs might be beneficial in treating painful intestinal disorders.

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“…The thoracic aorta was immediately isolated, freed from extraneous tissues and cut into multiple-ring preparations as previously described (Calderone et al 1996). The preparations were placed under a resting tension of 2 g in 10-mL organ baths at 37°C and continuously bubbled with a mixture of O 2 (95 % ) and CO 2 (5 % ).…”

Section: Experimental Protocolmentioning

confidence: 99%

Hormonal influence on the release of endothelial nitric oxide: gender-related dimorphic sensitivity of rat aorta for noradrenaline

Calderone

Baragatti

Breschi

et al. 2002

Journal of Pharmacy and Pharmacology

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Male gender shows a higher incidence of vascular disorders and this phenomenon could be explained by sexual dimorphic behaviour of vessels. Both gonadal hormones and endothelial nitric oxide (NO) are involved in the regulation of the vascular reactivity. This study aimed to evaluate a possible sexual dimorphic sensitivity of rat aorta for the catecholamine noradrenaline. To understand the role played by physiological concentrations of sex hormones, the experimental procedures were performed on isolated preparations from intact (sham-operated) and gonadectomized rats of both sexes. In parallel sets of experiments, the biosynthesis of NO was inhibited by N'-nitro-L-arginine methyl ester (L-NAME) to reveal any potential involvement of the endothelial modulator and its possible link with the endocrinous factor. In aortae from intact male and female rats, noradrenaline induced contractile effects with different potencies (mean+s.d. EC50 values 12.15 +/- 5.25 nM and 84.10 +/- 18.68 nM, respectively). Gonadectomy resulted in an increased sensitivity for noradrenaline in female vessels and a decreased sensitivity for the agonist in male vessels (EC50 values 25.64 +/- 5.04 nM and 21.70 +/ 1 1.13 nM, respectively). In aortae from intact male rats, the inhibition of NO biosynthesis resulted in a weak increase in sensitivity for noradrenaline (EC50 value 6.08 +/- 4.53 nM), whereas the increase was higher in vessels from intact female rats (EC50 value 10.38 +/- 8.40 nM). After treatment with L-NAME, aortae from gonadectomized male and female rats presented almost equivalent increases in sensitivity for the adrenergic agonist (EC50 values 6.02 +/- 3.63 nM and 9.10+/- 9.63 nM,respectively),and no significant difference in sensitivity could be recorded between intact and orchidectomized male rats, or between intact and ovariectomized female rats. It was concluded that rat aorta showed a sexual dimorphic sensitivity for noradrenaline and the female sex was more protected against the adrenergic contractile stimulus because of a higher release of endothelial NO. The gender-related difference in NO release was influenced by gonadal hormones, with the female hormones inducing an increase and the male hormones causing a reduction.

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A modified aortic multiple-ring preparation for functional studies

Cited by 19 publications

References 28 publications

H₂S-induced vasorelaxation and underlying cellular and molecular mechanisms

H₂S-induced vasorelaxation and underlying cellular and molecular mechanisms

Evidence That Hydrogen Sulfide Exerts Antinociceptive Effects in the Gastrointestinal Tract by Activating K_ATP Channels

Hormonal influence on the release of endothelial nitric oxide: gender-related dimorphic sensitivity of rat aorta for noradrenaline

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A modified aortic multiple-ring preparation for functional studies

Cited by 19 publications

References 28 publications

H2S-induced vasorelaxation and underlying cellular and molecular mechanisms

H2S-induced vasorelaxation and underlying cellular and molecular mechanisms

Evidence That Hydrogen Sulfide Exerts Antinociceptive Effects in the Gastrointestinal Tract by Activating KATP Channels

Hormonal influence on the release of endothelial nitric oxide: gender-related dimorphic sensitivity of rat aorta for noradrenaline

Contact Info

Product

Resources

About

H₂S-induced vasorelaxation and underlying cellular and molecular mechanisms

H₂S-induced vasorelaxation and underlying cellular and molecular mechanisms

Evidence That Hydrogen Sulfide Exerts Antinociceptive Effects in the Gastrointestinal Tract by Activating K_ATP Channels