Evidence of a decrease in nitric oxide-storage molecules following acute hypoxia and/or hypobaria, by means of chemiluminescence analysis

López-Ramos, Juan Carlos; Martínez-Romero, Rubén; Molina, Filomena; Cañuelo, Ana; Martı́nez-Lara, Esther; Siles, Eva; Peinado, M.A.

doi:10.1016/j.niox.2005.05.003

Cited by 42 publications

(28 citation statements)

References 21 publications

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“…Therefore, nitrate, nitrite and other compounds, which are stable metabolites of nitric oxide, are usually measured to determine nitric oxide production [31]. Many studies have been performed to directly measure vascular relaxation elicited by natural products and found that the vasorelaxant effect is related to stimulation of nitric oxide release from vascular tissues [32,33].…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular Effects Elicited by Milonine, a New 8,14‐Dihydromorphinandienone Alkaloid

Cavalcante

Ribeiro

Silva

et al. 2010

Basic Clin Pharma Tox

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Abstract:The mechanisms underlying the cardiovascular responses evoked by milonine (i.v.), an alkaloid, were investigated in rats. In normotensive rats, milonine injections produced hypotension and tachycardia, which were attenuated after N w -nitro-L-arginine methyl esther (L-NAME; 20 mg ⁄ kg, i.v.). In phenylephrine (10 lM), pre-contracted mesenteric artery rings, milonine (10 )10 M to 3 · 10 )4 M) caused a concentration-dependent relaxation (EC 50 = 1.1 · 10 )6 M, E max = 100 € 0.0%) and this effect was rightward shifted after either removal of the vascular endothelium (EC 50 = 1.6 · 10 )5, p < 0.001), or after L-NAME 100 lM (EC 50 = 6.2 · 10 , p < 0.001). Milonine also reduced CaCl 2 -induced contraction in Ca 2+ -free solution containing KCl (60 mM). In conclusion, using combined functional and biochemical approaches, we demonstrated that the hypotensive and vasorelaxant effects produced by milonine are, at least in part, mediated by the endothelium, likely via nitric oxide release, activation of nitric oxide-cGMP pathway and opening of K + channels.

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Section: Discussionmentioning

confidence: 99%

Cardiovascular Effects Elicited by Milonine, a New 8,14‐Dihydromorphinandienone Alkaloid

Cavalcante

Ribeiro

Silva

et al. 2010

Basic Clin Pharma Tox

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“…To further confirm such a hypothesis, a biochemical assay using a very sensitive technique for NOx analysis was performed (Chen, 1988;Braman et al, 1989). Since the half-life of NO is very short (a few seconds), nitrate, nitrite, and other nitroso compounds (NOxs), which are stable metabolites of NO, are frequently measured to determine NO production (López-Ramos et al, 2005). In endothelium-intact aorta rings pre-contracted with norepinephrine, DMF (10 −4 M) and acetylcholine (10 −5 M, used as positive control) significantly increased NOx levels.…”

Section: Discussionmentioning

confidence: 99%

Nitric oxide-dependent vasodilation and intracellular Ca2+ concentration increase induced by 6,8-dihydroxy-4-methoxyflavone in rat aorta

Fidegrave¹,

Ntchapda²,

Talla³

et al. 2013

J. Pharmacognosy Phytother.

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In this study, we attempted to evaluate the role of endothelium-derived hyperpolarizing factor (EDHF) in the vasorelaxant response induced by 6,8-Dihydroxy-4'-methoxyflavone (DMF) in isolated rat aorta rings by using functional and biochemical approaches. Thoracic aortic rings were isolated and suspended in organ baths, and the effects of DMF were studied by means of isometric tension recording experiments. Nitric oxide (NO) was detected by ozone-induced chemiluminescence. The technique used to evaluate changes in intracellular ([Ca 2+ ] i ) in intact endothelium was determined by open aortic ring and loaded with 16 µmol Fura-2/AM for 60 min at room temperature, washed and fixed by small pins with the luminal face up. In situ electrical conductivities (ECs) were visualized by an upright epifluorescence Axiolab microscope (Carl Zeiss, Oberkochen, Germany) equipped with a Zeiss × 63 Achroplan objective (water immersion, 2.0 mm working distance, 0.9 numerical apertures). ECs were excited alternately at 340 and 380 nm, and the emitted light was detected at 510 nm. In aortic rings with intact endothelium pre-contracted with norepinephrine (NE) (10 -4 M), the addition of DMF (10 −8 to 10 −4 M) induced vasorelaxation in a concentration-dependent manner; in endothelium-denuded rings, the relaxant response induced by DMF was almost completely abolished suggesting that vasorelaxation was endothelium-dependent. DMF (10 −4 M) was able to significantly increase NOx levels. This effect was completely abolished after removal of the vascular endothelium. DMF (100 µM) caused a slow, longlasting increase in [Ca 2+ ] i . These results further support the hypothesis that DMF can induce activation of the NO/sGC/cGMP pathway, as suggested by functional studies. The results of the present study, using combined functional and biochemical in vitro approaches, indicated that DMF relaxes precontracted isolated rat aortic rings. Such a vasorelaxation was an endothelium-dependent effect, via the NO/sGC/cGMP pathway. This result also suggests that DMF causes a slow influx of extracellular Ca 2+ . Release from the intracellular Ca 2+ stores and an inhibition of Ca 2+ extruding mechanisms.

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“…Since the half-life of NO in the body is very short, nitrate, nitrite, and other nitroso compounds (NO x s), which are stable metabolites of NO, are usually measured to determine NO production (47). In endothelium-intact superior mesenteric rings pre-contracted with phenylephrine, CMMTT (10 −6 M) and acetylcholine (10 −5 M, used as positive control) significantly increased NO x levels.…”

Section: Discussionmentioning

confidence: 99%

Endothelium-Derived Nitric Oxide Contributes to the Vasorelaxant Response Induced by Mesoionic 2-(4-Chlorophenyl)-3-methyl-4-(4-methoxyphenyl)-1;3-thiazolium-5-thyolate (CMMTT) in Rats

et al. 2009

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Abstract. This study was performed to investigate the mechanisms involved in the vasorelaxation induced by mesoionic 2-(4-chlorophenyl)-3-methyl-4-(4-methoxyphenyl)-1;3-thiazolium-5-thyolate (CMMTT), a newly synthesized mesoionic compound, in rat superior mesenteric arteries. In phenylephrine (10 μM)-pre-contracted mesenteric rings, CMMTT (10 −14 -10 −6 M) induced a concentration-dependent relaxation [pD 2 = 10.26 ± 0.05, E max = 80.8 ± 5.8%], and this effect was almost abolished after either removal of the vascular endothelium [E max = 17.7 ± 4.2%, P<0.001], removal of the vascular endothelium plus100 μM N ω -nitro-L-arginine methyl esther (L-NAME) [E max = 21.0 ± 2.0 %, P<0.001], or after pre-treatment of the rings with 100 μM L-NAME [E max = 13.3 ± 2.4%, P<0.001] or 10 μM 1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one (ODQ) [E max = 13.6 ± 4.8%, P<0.001]. However, endothelium-dependent relaxation induced by CMMTT was not significantly modified after 1 μM indomethacin plus 1 nM atropine [pD 2 = 11.12 ± 0.08, E max = 73.8 ± 5.15%] or 100 nM charybdotoxin (ChTX) plus 100 nM apamin [pD 2 = 10.89 ± 0.08, E max = 58.91 ± 9.8%]. In mesenteric rings, CMMTT (10 −6 M) was able to increase nitric oxide (NO) x levels, and this effect was abolished after removal of the vascular endothelium. In conclusion, the present study, using combined functional and biochemical approaches, demonstrated that CMMTT induced a significant vasorelaxant effect, almost completely mediated by the endothelium, likely via NO release and activation of the NO-cGMP pathway.

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Evidence of a decrease in nitric oxide-storage molecules following acute hypoxia and/or hypobaria, by means of chemiluminescence analysis

Cited by 42 publications

References 21 publications

Cardiovascular Effects Elicited by Milonine, a New 8,14‐Dihydromorphinandienone Alkaloid

Cardiovascular Effects Elicited by Milonine, a New 8,14‐Dihydromorphinandienone Alkaloid

Nitric oxide-dependent vasodilation and intracellular Ca2+ concentration increase induced by 6,8-dihydroxy-4-methoxyflavone in rat aorta

Endothelium-Derived Nitric Oxide Contributes to the Vasorelaxant Response Induced by Mesoionic 2-(4-Chlorophenyl)-3-methyl-4-(4-methoxyphenyl)-1;3-thiazolium-5-thyolate (CMMTT) in Rats

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