Conclusion
As a specific type of hypertensive disease during pregnancy, severe preeclampsia may be characterized by multiple factors, mechanisms and pathways. Our study investigated changes in the expression of TRPV1 and the KATP subtype SUR2B/Kir6.1 in placental arterioles in severe preeclampsia and the possible mechanism. However, further electrophysiological experiments are still necessary to further understand the etiology and pathogenesis of this disease and provide a new theoretical basis for the prevention, diagnosis and treatment of this disease.
Acknowledgements : Thanks to the medical Experiment Center platform of the Affiliated Hospital of Southwest Medical University for providing experimental site and experimental guidance.
Disclosure of Interests : The authors declare that they have no conflicts of interest.
Contribution to Authorship :
Zhou Xianyi: Conception and design, Acquisition of data, Analysis and Interpretation of data, Drafting of the manuscript, Statistical analysis.
Li Wei: Acquisition of data, Analysis and Interpretation of data, Drafting of the manuscript, Statistical analysis.
Lin Hairui: Conception and design, Acquisition of data, Analysis and Interpretation of data, Critical revision of the manuscript for important intellectual content , Statistical analysis.
Tan Yingyun: Conception and design, Acquisition of data, Analysis and Interpretation of data, Critical revision of the manuscript for important intellectual content , Statistical analysis.
Fu Xiaodong: Conception and design, Critical revision of the manuscript for important intellectual content, Obtaining funding, Supervision.
Details of Ethics Approval : This experiment was approved by the Clinical Trial Ethics Committee of the Affiliated Hospital of Southwest Medical University (registration number: KY2019039).
Funding : Luzhou Science and Technology Bureau: Expression and influence of KV7 channel in placental chorionic artery smooth muscle cells of pregnant women with fetal growth restriction due to preeclampsia (No.2020-SYF-27).
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37. Wu, Y., M.Y. He, J.K. Ye, et al., Activation of ATP-sensitive potassium channels facilitates the function of human endothelial colony-forming cells via Ca(2+) /Akt/eNOS pathway. J Cell Mol Med[J], 2017. 21 (3): p. 609-620.
1. Agrawal, A. and N.K. Wenger, Hypertension During Pregnancy.Curr Hypertens Rep, 2020. 22 (9): p. 64.
2. Hypertension in pregnancy. Report of the American College of Obstetricians and Gynecologists’ Task Force on Hypertension in Pregnancy. Obstet Gynecol, 2013. 122 (5): p. 1122-31.
3. Zhu, Z., Z. Luo, S. Ma, and D. Liu, TRP channels and their implications in metabolic diseases. Pflugers Arch, 2011.461 (2): p. 211-23.
4. Bratz, I.N., G.M. Dick, J.D. Tune, J.M. Edwards, Z.P. Neeb, U.D. Dincer, and M. Sturek, Impaired capsaicin-induced relaxation of coronary arteries in a porcine model of the metabolic syndrome. Am J Physiol Heart Circ Physiol, 2008. 294 (6): p. H2489-96.
5. Marshall, N.J., L. Liang, J. Bodkin, C. Dessapt-Baradez, M. Nandi, S. Collot-Teixeira, . . . S.D. Brain, A role for TRPV1 in influencing the onset of cardiovascular disease in obesity. Hypertension, 2013.61 (1): p. 246-52.
6. Yang, D., Z. Luo, S. Ma, W.T. Wong, L. Ma, J. Zhong, . . . Z. Zhu,Activation of TRPV1 by dietary capsaicin improves endothelium-dependent vasorelaxation and prevents hypertension. Cell Metab, 2010. 12 (2): p. 130-41.
7. Yokoshiki, H., M. Sunagawa, T. Seki, and N. Sperelakis,ATP-sensitive K+ channels in pancreatic, cardiac, and vascular smooth muscle cells. Am J Physiol, 1998. 274 (1): p. C25-37.
8. Lückhoff, A. and R. Busse, Activators of potassium channels enhance calcium influx into endothelial cells as a consequence of potassium currents. Naunyn Schmiedebergs Arch Pharmacol, 1990.342 (1): p. 94-9.
9. Lückhoff, A. and R. Busse, Calcium influx into endothelial cells and formation of endothelium-derived relaxing factor is controlled by the membrane potential. Pflugers Arch, 1990. 416 (3): p. 305-11.
10. Nelson, M.T., H. Cheng, M. Rubart, L.F. Santana, A.D. Bonev, H.J. Knot, and W.J. Lederer, Relaxation of arterial smooth muscle by calcium sparks. Science, 1995. 270 (5236): p. 633-7.
11. Guarini, G., V.A. Ohanyan, J.G. Kmetz, D.J. DelloStritto, R.J. Thoppil, C.K. Thodeti, . . . I.N. Bratz, Disruption of TRPV1-mediated coupling of coronary blood flow to cardiac metabolism in diabetic mice: role of nitric oxide and BK channels. Am J Physiol Heart Circ Physiol, 2012. 303 (2): p. H216-23.
12. Espinoza, J., A. Vidaeff, C.M. Pettker, H. Simhan, and G. Amer Coll Obstet, Gestational Hypertension and Preeclampsia. Obstetrics and Gynecology, 2020. 135 (6): p. E237-E260.
13. Moncada, S., R.M. Palmer, and E.A. Higgs, The discovery of nitric oxide as the endogenous nitrovasodilator. Hypertension, 1988.12 (4): p. 365-72.
14. Sumpio, B.E., J.T. Riley, and A. Dardik, Cells in focus: endothelial cell. Int J Biochem Cell Biol, 2002. 34 (12): p. 1508-12.
15. Konukoglu, D. and H. Uzun, Endothelial Dysfunction and Hypertension. Adv Exp Med Biol, 2017. 956 : p. 511-540.
16. Al-Magableh, M.R., B.K. Kemp-Harper, and J.L. Hart, Hydrogen sulfide treatment reduces blood pressure and oxidative stress in angiotensin II-induced hypertensive mice. Hypertens Res, 2015.38 (1): p. 13-20.
17. Ducat, A., L. Doridot, R. Calicchio, C. Mehats, J.L. Vilotte, J. Castille, . . . D. Vaiman, Endothelial cell dysfunction and cardiac hypertrophy in the STOX1 model of preeclampsia. Sci Rep, 2016.6 : p. 19196.
18. Pimentel, A.M.L., N.R. Pereira, C.A. Costa, G.E. Mann, V.S.C. Cordeiro, R.S. de Moura, . . . A.C. Resende, L-arginine-nitric oxide pathway and oxidative stress in plasma and platelets of patients with pre-eclampsia. Hypertension Research, 2013. 36 (9): p. 783-788.
19. Eleuterio, N.M., A.C.T. Palei, J.S.R. Machado, J.E. Tanus-Santos, R.C. Cavalli, and V.C. Sandrim, Relationship between adiponectin and nitrite in healthy and preeclampsia pregnancies. Clinica Chimica Acta, 2013. 423 : p. 112-115.
20. Sandrim, V.C., A.C.T. Palei, I.F. Metzger, V.A. Gomes, R.C. Cavalli, and J.E. Tanus-Santos, Nitric oxide formation is inversely related to serum levels of antiangiogenic factors soluble fms-like tyrosine kinase-1 and soluble endogline in preeclampsia. Hypertension, 2008.52 (2): p. 402-407.
21. Boeldt, D.S. and I.M. Bird, Vascular adaptation in pregnancy and endothelial dysfunction in preeclampsia. Journal of Endocrinology, 2017. 232 (1): p. R27-R44.
22. Osol, G., N.L. Ko, and M. Mandalà, Altered Endothelial Nitric Oxide Signaling as a Paradigm for Maternal Vascular Maladaptation in Preeclampsia. Curr Hypertens Rep, 2017. 19 (10): p. 82.
23. Brosens, I., A STUDY OF THE SPIRAL ARTERIES OF THE DECIDUA BASALIS IN NORMOTENSIVE AND HYPERTENSIVE PREGNANCIES. The Journal of obstetrics and gynaecology of the British Commonwealth, 1964.71 : p. 222-30.
24. Caterina, M.J., M.A. Schumacher, M. Tominaga, T.A. Rosen, J.D. Levine, and D. Julius, The capsaicin receptor: a heat-activated ion channel in the pain pathway. Nature, 1997. 389 (6653): p. 816-24.
25. Caterina, M.J., Vanilloid receptors take a TRP beyond the sensory afferent. Pain, 2003. 105 (1-2): p. 5-9.
26. Yang, X.R., M.J. Lin, L.S. McIntosh, and J.S. Sham, Functional expression of transient receptor potential melastatin- and vanilloid-related channels in pulmonary arterial and aortic smooth muscle. Am J Physiol Lung Cell Mol Physiol, 2006. 290 (6): p. L1267-76.
27. Zsombok, A., Vanilloid receptors–do they have a role in whole body metabolism? Evidence from TRPV1. J Diabetes Complications, 2013. 27 (3): p. 287-92.
28. Gunthorpe, M.J. and A. Szallasi, Peripheral TRPV1 receptors as targets for drug development: new molecules and mechanisms. Curr Pharm Des, 2008. 14 (1): p. 32-41.
29. Xin, H., H. Tanaka, M. Yamaguchi, S. Takemori, A. Nakamura, and K. Kohama, Vanilloid receptor expressed in the sarcoplasmic reticulum of rat skeletal muscle. Biochem Biophys Res Commun, 2005.332 (3): p. 756-62.
30. Song, M.Y. and J.X. Yuan, Introduction to TRP channels: structure, function, and regulation. Adv Exp Med Biol, 2010.661 : p. 99-108.
31. Cai, H., M.E. Davis, G.R. Drummond, and D.G. Harrison,Induction of endothelial NO synthase by hydrogen peroxide via a Ca(2+)/calmodulin-dependent protein kinase II/janus kinase 2-dependent pathway. Arterioscler Thromb Vasc Biol, 2001. 21 (10): p. 1571-6.
32. Zhang, M. and H.J. Vogel, Characterization of the calmodulin-binding domain of rat cerebellar nitric oxide synthase. J Biol Chem, 1994. 269 (2): p. 981-5.
33. Zhang, M., T. Yuan, J.M. Aramini, and H.J. Vogel, Interaction of calmodulin with its binding domain of rat cerebellar nitric oxide synthase. A multinuclear NMR study. J Biol Chem, 1995.270 (36): p. 20901-7.
34. Torres-Narváez, J.C., I. Pérez-Torres, V. Castrejón-Téllez, E. Varela-López, V.H. Oidor-Chan, V. Guarner-Lans, . . . L. Del Valle-Mondragón, The Role of the Activation of the TRPV1 Receptor and of Nitric Oxide in Changes in Endothelial and Cardiac Function and Biomarker Levels in Hypertensive Rats. Int J Environ Res Public Health, 2019. 16 (19).
35. Nieves-Cintrón, M., A.U. Syed, M.A. Nystoriak, and M.F. Navedo,Regulation of voltage-gated potassium channels in vascular smooth muscle during hypertension and metabolic disorders. Microcirculation, 2018. 25 (1).
36. Jackson, W.F., K(V) channels and the regulation of vascular smooth muscle tone. Microcirculation, 2018. 25 (1).
37. Wu, Y., M.Y. He, J.K. Ye, S.Y. Ma, W. Huang, Y.Y. Wei, . . . W.P. Xie, Activation of ATP-sensitive potassium channels facilitates the function of human endothelial colony-forming cells via Ca(2+) /Akt/eNOS pathway. J Cell Mol Med, 2017. 21 (3): p. 609-620.