ArticleBioMed research international2013
Ropivacaine-induced contraction is attenuated by both endothelial nitric oxide and voltage-dependent potassium channels in isolated rat aortae.
Article in BioMed research international, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 19 citations in OpenAlex.
- Direct effect of lipid emulsion treatment on local anesthetic systemic toxicity.Clinical and experimental emergency medicine · 2024Article
- Mechanisms underlying lipid emulsion resuscitation for drug toxicity: a narrative review.Korean journal of anesthesiology · 2023Review
- Mechanisms and Efficacy of Intravenous Lipid Emulsion Treatment for Systemic Toxicity From Local Anesthetics.Frontiers in medicine · 2021Review
- Nitric oxide-mediated inhibition of phenylephrine-induced contraction in response to hypothermia is partially modulated by endothelial Rho-kinase.International journal of medical sciences · 2020Article
- Linoleic Acid Attenuates the Toxic Dose of Bupivacaine-Mediated Reduction of Vasodilation Evoked by the Activation of Adenosine Triphosphate-Sensitive Potassium Channels.International journal of molecular sciences · 2018Article
- Lipid Emulsion for Treating Local Anesthetic Systemic Toxicity.International journal of medical sciences · 2018Review
- Possible mechanisms involved in the vasorelaxant effect produced by clobenzorex in aortic segments of rats.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2017Article
- A Lipid Emulsion Reverses Toxic-Dose Bupivacaine-Induced Vasodilation during Tyrosine Phosphorylation-Evoked Contraction in Isolated Rat Aortae.International journal of molecular sciences · 2017Article
- Lipid emulsion inhibits vasodilation induced by a toxic dose of bupivacaine by suppressing bupivacaine-induced PKC and CPI-17 dephosphorylation but has no effect on vasodilation induced by a toxic dose of mepivacaine.The Korean journal of pain · 2016Article
- Pharmacological study of the mechanisms involved in the vasodilator effect produced by the acute application of triiodothyronine to rat aortic rings.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2016Article
- Time-dependent changes in inhibitory action of lipopolysaccharide on intestinal motility in rat.The Journal of veterinary medical science · 2015Article
- The effect of mepivacaine on swine lingual, pulmonary and coronary arteries.BMC anesthesiology · 2015Article
- Pharmacological characterization of mechanisms involved in the vasorelaxation produced by rosuvastatin in aortic rings from rats with a cafeteria-style diet.Clinical and experimental pharmacology & physiology · 2015Article
- Lipid Emulsion Attenuates Acetylcholine-Induced Relaxation in Isolated Rat Aorta.BioMed research international · 2015Article
- Systemic blockage of nitric oxide synthase by L-NAME increases left ventricular systolic pressure, which is not augmented further by Intralipid®.International journal of biological sciences · 2014Article
- Linolenic Acid Attenuates the Vasodilation Induced by Acetylcholine in Isolated Rat Aortae.Dose-response : a publication of International Hormesis SocietyArticle
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study investigated endothelium-derived vasodilators and potassium channels involved in the modulation of ropivacaine-induced contraction. In endothelium-intact rat aortae, ropivacaine concentration-response curves were generated in the presence or absence of the following inhibitors: the nonspecific nitric oxide synthase (NOS) inhibitor N (ω) -nitro-L-arginine methyl ester (L-NAME), the neuronal NOS inhibitor N (ω) -propyl-L-arginine hydrochloride, the inducible NOS inhibitor 1400W dihydrochloride, the nitric oxide-sensitive guanylyl cyclase (GC) inhibitor ODQ, the NOS and GC inhibitor methylene blue, the phosphoinositide-3 kinase inhibitor wortmannin, the cytochrome p450 epoxygenase inhibitor fluconazole, the voltage-dependent potassium channel inhibitor 4-aminopyridine (4-AP), the calcium-activated potassium channel inhibitor tetraethylammonium (TEA), the inward-rectifying potassium channel inhibitor barium chloride, and the ATP-sensitive potassium channel inhibitor glibenclamide. The effect of ropivacaine on endothelial nitric oxide synthase (eNOS) phosphorylation in human umbilical vein endothelial cells was examined by western blotting. Ropivacaine-induced contraction was weaker in endothelium-intact aortae than in endothelium-denuded aortae. L-NAME, ODQ, and methylene blue enhanced ropivacaine-induced contraction, whereas wortmannin, N (ω) -propyl-L-arginine hydrochloride, 1400W dihydrochloride, and fluconazole had no effect. 4-AP and TEA enhanced ropivacaine-induced contraction; however, barium chloride and glibenclamide had no effect. eNOS phosphorylation was induced by ropivacaine. These results suggest that ropivacaine-induced contraction is attenuated primarily by both endothelial nitric oxide and voltage-dependent potassium channels.
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