Cyclooxygenase inhibitors depress norepinephrine constriction of rat abdominal, but not thoracic, aorta

Lamb, Victoria L.; Schwartz, Arthur G.; Rohn, William R.; Kaiser, Lana

doi:10.1016/0014-2999(94)90250-x

Cited by 23 publications

(16 citation statements)

References 12 publications

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“…These results seem to indicate that, in WKY and SHR aortas, the cyclooxygen ase inhibitors can interfere in a nonspecific way with the contractility of vascular smooth muscle. Similar results have been recently reported [34], suggesting that prosta noids may be involved in the contractile mechanisms elic ited by different vasoactive agents. These unexpected effects are not sufficient to discard the possibility that prostanoids could be involved in the endothelial modula tion of the ouabain-induced contractions.…”

Section: Discussionsupporting

confidence: 77%

Endothelial Modulation of Ouabain-lnduced Contraction and Sodium Pump Activity in Aortas of Normotensive Wystar-Kyoto and Spontaneously Hypertensive Rats

Ponte

Marı́n²,

Arribas³

et al. 1996

J Vasc Res

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The influence of vascular endothelium on ouabain-induced contractions and sodium pump activity in aortic segments of Wistar-Kyoto (WKY) and spontaneously hypertensive rat (SHR) was analyzed. De-endothelialization increased and reduced ouabain-induced contractions in WKY and SHR segments, respectively. The effects of de-endothelialization were not reproduced by pretreatment of the segments with N^G-nitro-L-arginine methyl ester, indo-methacin, or 5, 8, 11, 14-eicosatetraenoic acid, acetyl salicylic acid, dazoxiben, phosphoramidon, BQ-123, or superoxide dismutase. Bioassay experiments suggest that ouabain releases a diffusible factor from endothelial cells that inhibits or facilitates digitalis-induced contractions in WKY and SHR segments, respectively. In a potassium-free solution, potassium-induced relaxation in segments of both strains was abolished by ouabain in de-endothelialized aortas and reduced in intact ones. Ouabain-sensitive ⁸⁶Rb⁺ uptake was significantly reduced by de-endothelialization both in WKY and in SHR. These results suggest that the vascular endothelium of WKY and SHR aortas releases a diffusible factor that stimulates the sodium pump and/or protects it from ouabain blockade. Ouabain also releases a diffusible endothelium-derived factor in SHR aortas that facilitates ouabain-induced contractions.

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Section: Discussionsupporting

confidence: 77%

Endothelial Modulation of Ouabain-lnduced Contraction and Sodium Pump Activity in Aortas of Normotensive Wystar-Kyoto and Spontaneously Hypertensive Rats

Ponte

Marı́n²,

Arribas³

et al. 1996

J Vasc Res

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“…This suggests that, in the presence of indomethacin, the synergistic interaction between locally produced vasoconstrictor prostanoids and phenylephrine may be blocked, resulting in a consequent reduction of the effects of phenylephrine. Moreover, the effects of indomethacin on the vascular responsiveness to phenylephrine were observed both in preparations with and without endothelium, supporting previous studies that demonstrated a synergistic participation of non-endothelial vasoconstrictor prostanoids in the contractile actions of norepinephrine in rat mesenteric arteries (Peredo, 2001;Peredo, 2003) and aorta (Lamb et al, 1994) and of phenylephrine in rat aorta (Connoly et al, 1998).…”

Section: Discussionsupporting

confidence: 73%

Phenylephrine-induced vasoconstriction of the rat superior mesenteric artery is decreased after repeated swimming

Chies

Oliveira²,

Pereira³

et al. 2004

J. Smooth Muscle Res.

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This study was performed to determine the effect of forced swimming on the vascular responsiveness of the rat superior mesenteric artery to phenylephrine, focusing on the involvement of locally produced substances. Repeated but not single sessions of forced swimming exercise reduced the vasoconstrictor potency of phenylephrine in the studied arteries, regardless of the presence of intact endothelium. No significant changes were observed in the maximal response to phenylephrine. Treatment with indomethacin (1 µM) did not affect the exercise-induced reduction in vascular responsiveness to phenylephrine. However, the reduction of vascular reactivity to phenylephrine due to repeated exercise was no longer observed after treatment with N G -monomethyl-Larginine (L-NMMA, 100 µM). The results suggest that repeated exercise reduces vasomotor responses to phenylephrine in rat superior mesenteric arteries through a nonendothelial nitric oxide (NO)-related mechanism.

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“…O mecanismo do efeito vasoconstritor da norepinefrina é diferente na aorta torácica e abdominal sendo nesta última, mediada em parte, por um metabólito da cicloxigenase (Lamb et al 1994). Com relação ao tipo de preparação utilizada, Jansakul (1995) trabalhou com anéis enquanto que Edwards et al (1985) utilizaram tiras helicoidais de aortas de ratos.…”

Section: Discussionunclassified

A natação forçada induz subsensibilidade à fenilefrina em aorta torácica de rato

Moura¹,

Quintal²,

Marcondes³

2003

Rev. Bras. Cienc. Farm.

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Cyclooxygenase inhibitors depress norepinephrine constriction of rat abdominal, but not thoracic, aorta

Cited by 23 publications

References 12 publications

Endothelial Modulation of Ouabain-lnduced Contraction and Sodium Pump Activity in Aortas of Normotensive Wystar-Kyoto and Spontaneously Hypertensive Rats

Endothelial Modulation of Ouabain-lnduced Contraction and Sodium Pump Activity in Aortas of Normotensive Wystar-Kyoto and Spontaneously Hypertensive Rats

Phenylephrine-induced vasoconstriction of the rat superior mesenteric artery is decreased after repeated swimming

A natação forçada induz subsensibilidade à fenilefrina em aorta torácica de rato

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