Phosphatidylinositol 3-kinase inhibition induces vasodilator effect of sevoflurane via reduction of Rho kinase activity

Life Sciences

Volumn 177, Issue , 2017, Pages 20-26

  Miyamoto, Yasunori ^a   Feng, Guo Gang ^a   Satomi, Shiho ^b   Tanaka, Katsuya ^b   Fujiwara, Yoshihiro ^a   Kinoshita, Hiroyuki ^a,b  

^a AICHI MEDICAL UNIVERSITY SCHOOL OF MEDICINE   (Japan)

^b TOKUSHIMA UNIVERSITY HOSPITAL   (Japan)

Author keywords

Anesthetics; Phosphatidylinositol 3 kinase; Rho kinase; Sevoflurane

Indexed keywords

2 MORPHOLINO 8 PHENYLCHROMONE; MITOGEN ACTIVATED PROTEIN KINASE; PHENYLEPHRINE; PHOSPHATIDYLINOSITOL 3 KINASE; PROTEIN KINASE C; RHO KINASE; SEVOFLURANE; 2-(4-MORPHOLINYL)-8-PHENYL-4H-1-BENZOPYRAN-4-ONE; CHROMONE DERIVATIVE; ETHER DERIVATIVE; INHALATION ANESTHETIC AGENT; MORPHOLINE DERIVATIVE; VASODILATOR AGENT;

ANIMAL TISSUE; ARTERY CONSTRICTION; ARTICLE; BLOOD PRESSURE; CONTROLLED STUDY; ENZYME ACTIVITY; ENZYME INHIBITION; HEART RATE; HUMAN; HUMAN TISSUE; MALE; MEAN ARTERIAL PRESSURE; MESENTERIC ARTERY; NONHUMAN; RAT; VASODILATATION; AGED; ANIMAL; ANTAGONISTS AND INHIBITORS; AORTA; DRUG EFFECTS; INTRAVENOUS DRUG ADMINISTRATION; METABOLISM; MIDDLE AGED; VASOCONSTRICTION; WISTAR RAT;

AGED; ANESTHETICS, INHALATION; ANIMALS; AORTA; BLOOD PRESSURE; CHROMONES; HEART RATE; HUMANS; INJECTIONS, INTRAVENOUS; MALE; METHYL ETHERS; MIDDLE AGED; MITOGEN-ACTIVATED PROTEIN KINASES; MORPHOLINES; PHENYLEPHRINE; PHOSPHATIDYLINOSITOL 3-KINASE; PROTEIN KINASE C; RATS; RATS, WISTAR; RHO-ASSOCIATED KINASES; VASOCONSTRICTION; VASODILATOR AGENTS;

EID: 85017472009     PISSN: 00243205     EISSN: 18790631     Source Type: Journal    
DOI: 10.1016/j.lfs.2017.04.005     Document Type: Article

References (20)

1. [1] Wong, K.K., Engelman, J.A., Cantley, L.C., Targeting the PI3K signaling pathway in cancer. Curr. Opin. Genet. Dev. 20 (2010), 87–90.
2. [2] Ahmad, A., Biersack, B., Li, Y., Kong, D., Bao, B., Schobert, R., Padhye, S.B., Sarkar, F.H., Targeted regulation of PI3K/Akt/mTOR/NF-κB signaling by indole compounds and their derivatives: mechanistic details and biological implications for cancer therapy. Anti Cancer Agents Med. Chem. 13 (2013), 1002–1013.
3. [3] Morello, F., Perino, A., Hirsch, E., Phosphoinositide 3-kinase signaling in the vascular system. Cardiovasc. Res. 82 (2009), 261–271.
4. [4] Su, X., Smolock, E.M., Marcel, K.N., Moreland, R.S., Phosphatidylinositol 3-kinase modulates vascular smooth muscle contraction by calcium and myosin light chain phosphorylation-independent and -dependent pathways. Am. J. Phys. 286 (2004), H657–H666.
5. [5] Budzyn, K., Marley, P.D., Sobey, C.G., Opposing roles of endothelial and smooth muscle phosphatidylinositol 3-kinase in vasoconstriction: effects of rho-kinase and hypertension. J. Pharmacol. Exp. Ther. 313 (2005), 1248–1253.
6. [6] Yu, J., Ogawa, K., Tokinaga, Y., Hatano, Y., Sevoflurane inhibits guanosine 5′-[γ-thio]triphosphate-stimulated, Rho/Rho-kinase-mediated contraction of isolated rat aortic smooth muscle. Anesthesiology 99 (2003), 646–651.
7. 2 +-elicited contraction of rat aortic smooth muscle. Anesthesiology 100 (2004), 879–884.
8. [8] Yu, J., Mizumoto, K., Tokinaga, Y., Ogawa, K., Hatano, Y., The inhibitory effects of sevoflurane on angiotensin II-induced, p44/42 mitogen-activated protein kinase-mediated contraction of rat aortic smooth muscle. Anesth. Analg. 101 (2005), 315–321.
9. [9] Kinoshita, H., Matsuda, N., Kimoto, Y., Tohyama, S., Hama, K., Nakahata, K., Hatano, Y., Sevoflurane, but not propofol, prevents Rho kinase-dependent contraction induced by sphingosylphosphorylcholine in the porcine coronary artery. Anesth. Analg. 105 (2007), 325–329.
10. [10] Vinh, V.H., Enoki, T., Hirata, S., Toda, H., Kakuyama, M., Nakamura, K., Fukuda, K., Comparative contractile effects of halothane and sevoflurane in rat aorta. Anesthesiology 92 (2000), 219–227.
11. 2 + changes in the diabetic rat aorta. Can. J. Anesth. 57 (2010), 1095–1101.
12. + channel function impaired by thromboxane. Anesthesiology 111 (2009), 279–286.
13. + channel function impaired by high glucose in the human artery. Hypertension 52 (2008), 507–513.
14. [14] Yamamoto, Y., Saito, T., Feng, G.-G., Li, J., Yasuda, Y., Kazaoka, Y., Fujiwara, Y., Kinoshita, H., Intermittent local periodontal inflammation causes endothelial dysfunction of the systemic artery via increased levels of hydrogen peroxide concomitantly with overexpression of superoxide dismutase. Int. J. Cardiol. 222 (2016), 901–907.
15. + channels. J. Pharmacol. Sci. 129 (2015), 31–37.
16. [16] Okuno, T., Changes in blood volume and potassium concentration during exercise in rats. Jpn. J. Physiol. 42 (1992), 779–792.
17. [17] Watanabe, S., Matsumoto, T., Oda, M., Yamada, K., Takagi, J., Taguchi, K., Kobayashi, T., Insulin augments serotonin-induced contraction via activation of the IR/PI3K/PDK1 pathway in the rat carotid artery. Pflugers Arch. - Eur. J. Physiol. 468 (2016), 667–677.
18. [18] Liu, H., Chen, Z., Liu, J., Liu, L., Gao, Y., Dou, D., Endothelium-independent hypoxic contraction of porcine coronary arteries may be mediated by activation of phosphoinositide 3-kinase/Akt pathway. Vasc. Pharmacol. 61 (2014), 56–62.
19. [19] Eger, E.I. II, Age, minimum alveolar anesthetic concentration, and minimum alveolar anesthetic concentration-awake. Anesth. Analg. 93 (2001), 947–953.
20. 2 pneumoperitoneum stimulus. Br. J. Anaesth. 114 (2015), 634–639.