Ropivacaine-Induced Contraction Is Attenuated by Both Endothelial Nitric Oxide and Voltage-Dependent Potassium Channels in Isolated Rat Aortae

Ok, Seong-Ho; Han, Jeong Yeol; Sung, Hui-Jin; Yang, Seong Min; Park, Jung Chul; Kwon, Seong-Chun; Choi, Mun-Jeoung; Sohn, Ju-Tae

doi:10.1155/2013/565271

Cited by 17 publications

(30 citation statements)

References 29 publications

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“…Levobupivaciane, ropivacaine, and mepivacaine induce endothelial NOS phosphorylation in human umbilical vein endothelial cells and rat aorta 11,12,34,36. In particular, ropivacaine-induced contraction is enhanced by the non-specific NOS inhibitor L-NAME in endothelium-intact aorta, whereas ropivacaine-induced contraction is not significantly affected by the neuronal NOS inhibitor N ω -propyl-L-arginine hydrochloride or the inducible NOS inhibitor 1400W dihydrochloride, suggesting that ropivacaine-induced contraction is attenuated by endothelial NOS 36. Local anesthetic toxicity produces myocardial depression and cardiac arrest 37.…”

Section: Discussionmentioning

confidence: 99%

Systemic Blockage of Nitric Oxide Synthase by L-NAME Increases Left Ventricular Systolic Pressure, Which Is Not Augmented Further by Intralipid^®

Shin¹,

Hah²,

Kim³

et al. 2014

Int. J. Biol. Sci.

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Intravenous lipid emulsions (LEs) are effective in the treatment of toxicity associated with various drugs such as local anesthetics and other lipid soluble agents. The goals of this study were to examine the effect of LE on left ventricular hemodynamic variables and systemic blood pressure in an in vivo rat model, and to determine the associated cellular mechanism with a particular focus on nitric oxide. Two LEs (Intralipid® 20% and Lipofundin® MCT/LCT 20%) or normal saline were administered intravenously in an in vivo rat model following induction of anesthesia by intramuscular injection of tiletamine/zolazepam and xylazine. Left ventricular systolic pressure (LVSP), blood pressure, heart rate, maximum rate of intraventricular pressure increase, and maximum rate of intraventricular pressure decrease were measured before and after intravenous administration of various doses of LEs or normal saline to an in vivo rat with or without pretreatment with the non-specific nitric oxide synthase inhibitor Nω-nitro-L-arginine-methyl ester (L-NAME). Administration of Intralipid® (3 and 10 ml/kg) increased LVSP and decreased heart rate. Pretreatment with L-NAME (10 mg/kg) increased LSVP and decreased heart rate, whereas subsequent treatment with Intralipid® did not significantly alter LVSP. Intralipid® (10 ml/kg) increased mean blood pressure and decreased heart rate. The increase in LVSP induced by Lipofundin® MCT/LCT was greater than that induced by Intralipid®. Intralipid® (1%) did not significantly alter nitric oxide donor sodium nitroprusside-induced relaxation in endothelium-denuded rat aorta. Taken together, systemic blockage of nitric oxide synthase by L-NAME increases LVSP, which is not augmented further by intralipid®.

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Section: Discussionmentioning

confidence: 99%

Systemic Blockage of Nitric Oxide Synthase by L-NAME Increases Left Ventricular Systolic Pressure, Which Is Not Augmented Further by Intralipid^®

Shin¹,

Hah²,

Kim³

et al. 2014

Int. J. Biol. Sci.

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“…The fact that vasorelaxant responses induced by 10 −9 –10 −5 ‐mol/L rosuvastatin in aortic rings of rats with CAF diet were unaffected by vehicle and significantly ( P < 0.05) attenuated by 10 −5 ‐mol/L l ‐NAME (a direct inhibitor of NOS), 10 −2 ‐mol/L TEA (a Ca 2+ ‐activated K + channel blocker and non‐specific voltage‐activated K + channel blocker), 10 −3 ‐mol/L 4‐AP (a voltage‐activated K + channel blocker), and 10 −7 ‐mol/L apamin plus 10 −7 ‐mol/L charybdotoxin (blockers of small‐ and large‐conductance Ca 2+ ‐activated K + channels, respectively) suggests the involvement of eNOS, Ca 2+ ‐activated K + channels, and to a lesser extent, voltage‐activated K + channels . The western blot analysis showed enhanced protein levels of iNOS and eNOS in aortic rings from rats with a CAF diet that were exposed to phenylephrine plus rosuvastatin, but not to phenylephrine alone.…”

Section: Discussionmentioning

confidence: 99%

Pharmacological characterization of mechanisms involved in the vasorelaxation produced by rosuvastatin in aortic rings from rats with a cafeteria‐style diet

López-Canales

Lozano-Cuenca

López-Canales

et al. 2015

Clin Exp Pharma Physio

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The present study aimed to investigate the possible influence of several inhibitors and blockers on the vascular effect produced by the acute in vitro application of rosuvastatin to phenylephrine-precontracted aortic rings from rats with a semi-solid, cafeteria-style (CAF) diet. It also aimed to examine the effects of rosuvastatin on the expression of endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase, constitutive cyclooxygenase, and inducible cyclooxygenase in aortic rings from rats with a CAF diet. From comparisons of the effect on phenylephrine-precontracted aortic rings extracted from rats with two different diets (a standard and a CAF diet), it was found that 10−9–10−5-mol/L rosuvastatin produced lower concentration-dependent vasorelaxation on rings from the CAF diet group. The vasorelaxant effect was unaffected by the vehicle, but it was significantly attenuated by 10−5-mol/L NG-nitro-l-arginine methyl ester, 10−2-mol/L tetraethylammonium, 10−3-mol/L 4-aminopyridine, 10−7-mol/L apamin plus 10−7-mol/L charybdotoxin, 10−5-mol/L indomethacin, or 10−5-mol/L cycloheximide. Moreover, in aortic rings from rats with a CAF diet, rosuvastatin enhanced the expression of eNOS, inducible nitric oxide synthase, constitutive cyclooxygenase, and inducible cyclooxygenase. The acute in vitro application of rosuvastatin to phenylephrine-precontracted aortic rings from rats with a CAF diet had a vasorelaxant effect. Overall, the present results suggest that the stimulation of eNOS, the opening of Ca2+-activated and voltage-activated K+ channels, the stimulation of prostaglandin synthesis and enhanced protein levels of eNOS, inducible nitric oxide synthase, constitutive cyclooxygenase, and inducible cyclooxygenase are involved in this relaxant effect.

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“…The fact that the vasorelaxant effect produced by clobenzorex was unaffected by glibenclamide (an ATP-sensitive K + channel blocker) ( 24 ) and 4-AP (a voltage-activated K + channel blocker) ( 25 , 26 ), but significantly attenuated by TEA (a Ca 2+ -activated K + channel blocker and non-specific voltage-activated K + channel blocker) ( 25 , 27 ) and apamin plus charybdotoxin (blockers of small- and large-conductance Ca 2+ -activated K + channels, respectively) ( 28 – 30 ) suggests the involvement of Ca 2+ -activated K + channels in the aforementioned effect. Furthermore, the vasorelaxant effect induced by clobenzorex was unaffected by distilled water (vehicle of L-NAME, 4-AP and TEA) and 1.73×10 -2 M acetic acid (vehicle of apamin plus charybdotoxin).…”

Section: Discussionmentioning

confidence: 99%

Possible mechanisms involved in the vasorelaxant effect produced by clobenzorex in aortic segments of rats

Lozano-Cuenca

González‐Hernández

López-Canales

et al. 2017

Braz J Med Biol Res

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Clobenzorex is a metabolic precursor of amphetamine indicated for the treatment of obesity. Amphetamines have been involved with cardiovascular side effects such as hypertension and pulmonary arterial hypertension. The aim of the present study was to investigate whether the direct application of 10–9–10–5 M clobenzorex on isolated phenylephrine-precontracted rat aortic rings produces vascular effects, and if so, what mechanisms may be involved. Clobenzorex produced an immediate concentration-dependent vasorelaxant effect at the higher concentrations (10–7.5–10–5 M). The present outcome was not modified by 10–6 M atropine (an antagonist of muscarinic acetylcholine receptors), 3.1×10–7 M glibenclamide (an ATP-sensitive K+ channel blocker), 10–3 M 4-aminopyridine (4-AP; a voltage-activated K+ channel blocker), 10–5 M indomethacin (a prostaglandin synthesis inhibitor), 10–5 M clotrimazole (a cytochrome P450 inhibitor) or 10–5 M cycloheximide (a general protein synthesis inhibitor). Contrarily, the clobenzorex-induced vasorelaxation was significantly attenuated (P<0.05) by 10–5 M L-NAME (a direct inhibitor of nitric oxide synthase), 10–7 M ODQ (an inhibitor of nitric oxide-sensitive guanylyl cyclase), 10–6 M KT 5823 (an inhibitor of protein kinase G), 10–2 M TEA (a Ca2+-activated K+ channel blocker and non-specific voltage-activated K+ channel blocker) and 10–7 M apamin plus 10–7 M charybdotoxin (blockers of small- and large-conductance Ca2+-activated K+ channels, respectively), and was blocked by 8×10–2 M potassium (a high concentration) and removal of the vascular endothelium. These results suggest that the direct vasorelaxant effect by clobenzorex on phenylephrine-precontracted rat aortic rings involved stimulation of the NO/cGMP/PKG/Ca2+-activated K+ channel pathway.

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Ropivacaine-Induced Contraction Is Attenuated by Both Endothelial Nitric Oxide and Voltage-Dependent Potassium Channels in Isolated Rat Aortae

Cited by 17 publications

References 29 publications

Systemic Blockage of Nitric Oxide Synthase by L-NAME Increases Left Ventricular Systolic Pressure, Which Is Not Augmented Further by Intralipid^®

Systemic Blockage of Nitric Oxide Synthase by L-NAME Increases Left Ventricular Systolic Pressure, Which Is Not Augmented Further by Intralipid^®

Pharmacological characterization of mechanisms involved in the vasorelaxation produced by rosuvastatin in aortic rings from rats with a cafeteria‐style diet

Possible mechanisms involved in the vasorelaxant effect produced by clobenzorex in aortic segments of rats

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Ropivacaine-Induced Contraction Is Attenuated by Both Endothelial Nitric Oxide and Voltage-Dependent Potassium Channels in Isolated Rat Aortae

Cited by 17 publications

References 29 publications

Systemic Blockage of Nitric Oxide Synthase by L-NAME Increases Left Ventricular Systolic Pressure, Which Is Not Augmented Further by Intralipid®

Systemic Blockage of Nitric Oxide Synthase by L-NAME Increases Left Ventricular Systolic Pressure, Which Is Not Augmented Further by Intralipid®

Pharmacological characterization of mechanisms involved in the vasorelaxation produced by rosuvastatin in aortic rings from rats with a cafeteria‐style diet

Possible mechanisms involved in the vasorelaxant effect produced by clobenzorex in aortic segments of rats

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Systemic Blockage of Nitric Oxide Synthase by L-NAME Increases Left Ventricular Systolic Pressure, Which Is Not Augmented Further by Intralipid^®

Systemic Blockage of Nitric Oxide Synthase by L-NAME Increases Left Ventricular Systolic Pressure, Which Is Not Augmented Further by Intralipid^®