Endothelium-dependent relaxation resistant to NG-nitro-l-arginine in rat aorta

Hatake, Kiyohiko; Wakabayashi, Ichiro; Hishida, Shigeru

doi:10.1016/0014-2999(94)00704-b

Cited by 26 publications

(18 citation statements)

References 33 publications

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“…A low-molecular-weight superoxide anion scavenger tiron abolished the indigo carmine-induced potentiation of contraction evoked by phenylephrine. These results, along with previous reports [6,7,[11][12][13], suggest that indigo carmine enhances the phenylephrine-induced contraction in the endothelium-intact rings via NO inactivation induced by indigo carmine-induced ROS production (Fig. 6).…”

Section: Indigo Carmine and Nitric Oxidesupporting

confidence: 88%

“…Enhanced production of O 2 • -increases NO inactivation [11], which leads to a decrease in endotheliumdependent NO-mediated relaxation. Endothelial NO was reported to inhibit the contractile agonist (e.g., phenylephrine and norepinephrine)-induced contraction of the rat aorta [12,13]. A low-molecular-weight superoxide anion scavenger tiron abolished the indigo carmine-induced potentiation of contraction evoked by phenylephrine.…”

Section: Indigo Carmine and Nitric Oxidementioning

confidence: 98%

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Indigo carmine enhances phenylephrine-induced contractions in an isolated rat aorta

Choi

Lee

et al. 2011

Korean J Anesthesiol

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Background:The intravenous administration of indigo carmine has been reported to produce transiently increased blood pressure in patients. The goal of this in vitro study was to examine the effect of indigo carmine on phenylephrine-induced contractions in an isolated rat aorta and to determine the associated cellular mechanism with particular focus on the endothelium-derived vasodilators. Methods:The concentration-response curves for phenylephrine were generated in the presence or absence of indigo carmine. Phenylephrine concentration-response curves were generated for the endothelium-intact rings pretreated independently with a nitric oxide synthase inhibitor, N ω -nitro-L-arginine methyl ester (L-NAME), a cyclooxygenase inhibitor, indomethacin, and a low-molecular-weight superoxide anion scavenger, tiron, in the presence or absence of indigo carmine. The fluorescence of oxidized dichlorofluorescein was measured in rat aortic vascular smooth muscle cells cultured in the control, indigo carmine alone and tiron plus indigo carmine. Results: Indigo carmine (10-5 M) increased the phenylephrine-induced maximum contraction in the endotheliumintact rings with or without indomethacin, whereas indigo carmine produced a slight leftward shift in the phenylephrine concentration-response curves in the endothelium-denuded rings and L-NAME-pretreated endothelium-intact rings. In the endothelium-intact rings pretreated with tiron (10 -2 M), indigo carmine did not alter phenylephrine concentration-response curves significantly. Indigo carmine (10 -5 M) increased the fluorescence of oxidized dichlorofluorescein in the vascular smooth muscle cells, whereas tiron abolished the indigo carmineinduced increase in oxidized dichlorofluorescein fluorescence. Conclusions:Indigo carmine increases the phenylephrine-induced contraction mainly through an endotheliumdependent mechanism involving the inactivation of nitric oxide caused by the increased production of reactive oxygen species. (Korean J Anesthesiol 2011; 61: 55-62)

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Section: Indigo Carmine and Nitric Oxidesupporting

confidence: 88%

Section: Indigo Carmine and Nitric Oxidementioning

confidence: 98%

Indigo carmine enhances phenylephrine-induced contractions in an isolated rat aorta

Choi

Lee

et al. 2011

Korean J Anesthesiol

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“…In addition, EDHF causes endothelium-dependent relaxation in the rat aorta, which is resistant to the full blockade of NOS and cyclooxygenase (12). Previous studies (12,13) reported that NO inhibits the contractile agonist-induced contraction of rat aorta.…”

Section: Discussionmentioning

confidence: 97%

Diazepam Attenuates Phenylephrine-Induced Contractions in Rat Aorta

Park¹,

Sohn²,

Kim³

et al. 2006

Anesthesia & Analgesia

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In this in vitro study we examined the effects of diazepam on a phenylephrine-induced contraction in rat aorta and determined the associated cellular mechanism focusing on the endothelium-derived vasodilators. The concentration-response curves for phenylephrine and potassium chloride were generated in the presence or absence of diazepam. Phenylephrine concentration-response curves were generated from the endothelium-intact rings pretreated independently with N(W)-nitro-L-arginine methyl ester, PK 11195, tetraethylammonium, and indomethacin in the presence or absence of diazepam. Diazepam (7 x 10(-7) M) attenuated the phenylephrine-induced contraction in the endothelium-intact rings, whereas a large dose (5 x 10(-6) M) of diazepam attenuated the phenylephrine-induced contraction in the aortic rings with or without the endothelium. A pretreatment with the N(W)-nitro-L-arginine methyl ester completely abolished the diazepam (7 x 10(-7) M)-induced attenuation of the phenylephrine concentration-response curve, as well as the diazepam (5 x 10(-6) M)-induced attenuation of the maximal contractile response to phenylephrine. The N(W)-nitro-L-arginine methyl ester (10(-4) M)-induced contraction was enhanced in the rings pretreated with diazepam (5 x 10(-6) M). These results indicate that a supraclinical concentration of diazepam attenuates phenylephrine-induced contraction by increasing endothelial nitric oxide activity and directly affecting vascular smooth muscle.

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“…1e; cf. Hatake et al 1995). In additional experiments, the substrate of nitric oxide synthase, L-arginine (10 mM), was added 45 min before the second precontraction by noradrenaline (0.01 µM), followed by L-NAME (30 µM) 30 min before the second precontraction.…”

Section: Relaxation: Generalmentioning

confidence: 99%

Characterization by antagonists of P2-receptors mediating endothelium-dependent relaxation in the rat aorta

Hansmann

Bültmann

Tuluc

et al. 1997

Naunyn-Schmiedeberg's Arch Pharmacol

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The receptors through which 2-methylthio ATP (MeSATP), adenosine 5'-O-(2-thiodiphosphate) (ADP beta S), UTP and ATP elicit endothelium-dependent relaxation of noradrenaline-precontracted rings of the rat aorta were characterized by means of a series of antagonists. The acetylcholine-induced relaxation and the degradation of MeSATP, UTP and ATP were also studied. The potency of the nucleotides at producing relaxation decreased in the order MeSATP (EC50 0.24 microM) > ADP beta S (0.43 microM) > UTP (1.09 microM) > ATP (3.53 microM). MeSATP, ADP beta S and UTP did not cause relaxation when the endothelium had been destroyed; high concentrations of ATP still caused some relaxation. The relaxation by MeSATP, ADP beta S and UTP became very small after treatment of the rings with NG-nitro-L-arginine methyl ester; the relaxation by ATP was less affected. Pre-exposure to MeSATP (100 microM) abolished or almost abolished the relaxation normally elicited by MeSATP and ADP beta S, did not change that elicited by UTP and slightly enhanced the relaxation elicited by ATP. Of nine compounds examined as antagonists, six attenuated selectively the effect of some or all of the nucleotides (as compared to acetylcholine): suramin, reactive blue 2, pyridoxalphosphate-6-azophenyl-2',5'-disulphonate (iso-PPADS), pyridoxalphosphate-6-azophenyl-2',4'-disulphonate (PPADS), reactive red 2 and 5,5'-(1,1'-biphenyl-4,4'-diylbisazo)-bis-7-amino -6-hydroxy-naphthalene-1,4-disulphonate (NH05). Decreases of maximal relaxations and slopes different from unity in Schild plots often indicated non-competitive kinetics of the antagonism. For each of the six 'selective' antagonist, the apparent Kd values against MeSATP and against ADP beta S were similar: none of the six differentiated between MeSATP and ADP beta S. Also, for each of four 'selective' antagonists, the apparent Kd values against UTP and against ATP were similar: none of the four differentiated between these two nucleotides (two antagonists did not act against UTP and ATP in the 'selective' concentration range). On the other hand, for five of the six 'selective' antagonists (the exception being NH05), the apparent Kd values against MeSATP and ADP beta S were considerably lower than those against UTP and ATP. At the highest concentrations tested against agonist-evoked relaxations, the antagonists did not alter the removal from the incubation medium, by pieces of rat aorta, of MeSATP, UTP and ATP. It is concluded that nucleotides cause endothelium-dependent relaxation of the rat aorta through two sites: a P2Y-receptor and a P2U-receptor. The receptors may be pharmacologically similar to a bovine endothelial P2Y (P2Y1) and a cloned rat P2U (P2Y2) receptor, respectively. ATP acts mainly through the P2U-receptor. Suramin, reactive blue 2, iso-PPADS, PPADS and reactive red 2 are more potent at the P2Y- than the P2U-receptor. NH05 does not discriminate between the two receptors but is the most potent P2U antagonist so far described.

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Endothelium-dependent relaxation resistant to NG-nitro-l-arginine in rat aorta

Cited by 26 publications

References 33 publications

Indigo carmine enhances phenylephrine-induced contractions in an isolated rat aorta

Indigo carmine enhances phenylephrine-induced contractions in an isolated rat aorta

Diazepam Attenuates Phenylephrine-Induced Contractions in Rat Aorta

Characterization by antagonists of P2-receptors mediating endothelium-dependent relaxation in the rat aorta

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