Linolenic acid enhances contraction induced by phenylephrine in isolated rat aorta.

@article{Lee2020LinolenicAE,
  title={Linolenic acid enhances contraction induced by phenylephrine in isolated rat aorta.},
  author={Soo Hee Lee and Seong-chun Kwon and Seong-Ho Ok and Seung Hyun Ahn and Sung Il Bae and Yeran Hwang and Kyeong Eon Park and Ju-Tae Sohn},
  journal={European journal of pharmacology},
  year={2020},
  pages={
          173662
        }
}

Lipid Emulsion Enhances Vasoconstriction Induced by Dexmedetomidine in the Isolated Endothelium-Intact Aorta

  • S. LeeS. Ok J. Sohn
  • Biology, Chemistry
    International journal of molecular sciences
  • 2021
LE enhanced the DMT-induced contraction by inhibition of NO synthesis, which may be caused by the decreased DMT concentration, and the effect of LE was examined in the human umbilical vein endothelial cells.

References

SHOWING 1-10 OF 35 REFERENCES

Linolenic Acid Attenuates the Vasodilation Induced by Acetylcholine in Isolated Rat Aortae

  • S. LeeS. Ok J. Sohn
  • Biology, Chemistry
    Dose-response : a publication of International Hormesis Society
  • 2019
Results suggest that linolenic acid inhibits acetylcholine-induced relaxation by inhibiting a step just prior to nitric oxide-induced cGMP formation, which seems to be partially associated with inhibition of the Nitric oxide–cGMP pathway.

Lipofundin MCT/LCT Inhibits Levcromakalim-Induced Vasodilation by Inhibiting Endothelial Nitric Oxide Release

Results suggest that Lipofundin MCT/LCT inhibits the vasodilation induced by levcromakalim by inhibiting basally released endothelial nitric oxide, which seems to occur through medium-chain fatty acids.

Lipid Emulsion Attenuates Acetylcholine-Induced Relaxation in Isolated Rat Aorta

Taken together, Lipofundin MCT/LCT attenuated acetylcholine-induced NO-mediated relaxation via an inhibitory effect on the endothelium including eNOS, which is proximal to activation of guanylyl cyclase.

Dexmedetomidine-induced contraction of isolated rat aorta is dependent on extracellular calcium concentration

Background Dexmedetomidine is a highly selective α2-adrenoceptor agonist that is widely used for sedation and analgesia during the perioperative period. Intravenous administration of dexmedetomidine

Dexmedetomidine Inhibits Phenylephrine-induced Contractions via Alpha-1 Adrenoceptor Blockade and Nitric Oxide Release in Isolated Rat Aortae

  • H. ByonS. Ok J. Sohn
  • Biology, Medicine
    International journal of medical sciences
  • 2017
It is suggested that dexmedetomidine attenuates phenylephrine-induced contractions via alpha-1 adrenoceptor blockade and endothelial nitric oxide release in the isolated rat aorta via rauwolscine.

Effect of arachidonic acid on the L‐type calcium current in frog cardiac myocytes.

The results suggest that neither a PKC‐ nor a G‐protein‐mediated mechanism are likely to be involved in the effect of AA on ICa,L, and that this process could provide a new mechanism in the modulation of calcium channel activity.

The effect of sugammadex on the vascular tone of isolated rat aorta

The results suggest that sugammadex itself, in a dose that exceeds the clinical dose of sugamadex (10 M), has no direct effect on voltageor receptor-operated calcium channels or endothelium-derived vasodilators, including nitric oxide, which contribute to vascular tone modulation.

A Lipid Emulsion Reverses Toxic-Dose Bupivacaine-Induced Vasodilation during Tyrosine Phosphorylation-Evoked Contraction in Isolated Rat Aortae

  • S. OkS. Lee J. Sohn
  • Biology, Chemistry
    International journal of molecular sciences
  • 2017
It is suggested that a lipid emulsion reverses toxic-dose bupivacaine-induced vasodilation during sodium orthovanadate-induced contraction via the activation of a pathway involving either tyrosine kinase, JNK, Rho-kinase and MYPT1 or tyOSin phosphatase, PLC γ-1 and ERK and this reversal is associated with the lipid solubility of the local anesthetic and the induction of calcium sensitization.

Nitric Oxide Induces Dilation of Rat Aorta via Inhibition of Rho-Kinase Signaling

The hypothesis that endogenous NO-mediated vasodilation occurs through the inhibition of Rho-kinase constrictor activity in the intact rat aorta is supported.