Endothelin and neonatal capsaicin regulate gastric resistance to injury in BDL rats

Câmara, Paula Rs; Ferraz, Gerson J. N.; Velloso, Lı́cio A.; Zeitune, José Murilo Robilotta; Suassuna, Fernando Ab; Ferraz, José G.

doi:10.4291/wjgp.v3.i4.85

Cited by 4 publications

(1 citation statement)

References 27 publications

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“…The effects of local SNAC, NaNO 2 and NaNO 3 solution administration on GMBF were measured using the ex vivo gastric chamber method described by Camara et al [32]. A pencil probe (type N, penetration 1 mm, Transonic Systems, Ithaca, NY, USA) connected to a Laser Doppler Flowmeter (BLF 21A, Transonic Systems) was used in all cases.…”

Section: Methodsmentioning

confidence: 99%

Nitric Oxide Released from Luminal S-Nitroso-N-Acetylcysteine Increases Gastric Mucosal Blood Flow

et al. 2015

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Nitric oxide (NO)-mediated vasodilation plays a key role in gastric mucosal defense, and NO-donor drugs may protect against diseases associated with gastric mucosal blood flow (GMBF) deficiencies. In this study, we used the ex vivo gastric chamber method and Laser Doppler Flowmetry to characterize the effects of luminal aqueous NO-donor drug S-nitroso-N-acetylcysteine (SNAC) solution administration compared to aqueous NaNO2 and NaNO3 solutions (pH 7.4) on GMBF in Sprague-Dawley rats. SNAC solutions (600 μM and 12 mM) led to a rapid threefold increase in GMBF, which was maintained during the incubation of the solutions with the gastric mucosa, while NaNO2 or NaNO3 solutions (12 mM) did not affect GMBF. SNAC solutions (600 μM and 12 mM) spontaneously released NO at 37 °C at a constant rate of 0.3 or 14 nmol·mL, respectively, while NaNO2 (12 mM) released NO at a rate of 0.06 nmol·mLand NaNO3 (12 mM) did not release NO. These results suggest that the SNAC-induced GMBF increase is due to their higher rates of spontaneous NO release compared to equimolar NaNO2 solutions. Taken together, our data indicate that oral SNAC administration is a potential approach for gastric acid-peptic disorder prevention and treatment.

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Section: Methodsmentioning

confidence: 99%

Nitric Oxide Released from Luminal S-Nitroso-N-Acetylcysteine Increases Gastric Mucosal Blood Flow

et al. 2015

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Blockade of endothelin ETA, but not thromboxane, receptors offsets the cyclosporine-evoked hypertension and interrelated baroreflex and vascular dysfunctions

Nasser

El-Mallah

Sabra

et al. 2014

European Journal of Pharmacology

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Facilitation by the renin-angiotensin system of cyclosporine-evoked hypertension in rats: Role of arterial baroreflexes and vasoreactivity

et al. 2016

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Endothelin and neonatal capsaicin regulate gastric resistance to injury in BDL rats

Abstract: Our results suggest that the reduced resistance of the gastric mucosa of cirrhotic rats to ethanol-induced injury is a phenomenon modulated by ET through the ET(B) receptor and by sensory afferent neurons.

Cited by 4 publications

References 27 publications

Nitric Oxide Released from Luminal S-Nitroso-N-Acetylcysteine Increases Gastric Mucosal Blood Flow

Nitric Oxide Released from Luminal S-Nitroso-N-Acetylcysteine Increases Gastric Mucosal Blood Flow

Blockade of endothelin ETA, but not thromboxane, receptors offsets the cyclosporine-evoked hypertension and interrelated baroreflex and vascular dysfunctions

Facilitation by the renin-angiotensin system of cyclosporine-evoked hypertension in rats: Role of arterial baroreflexes and vasoreactivity

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