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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pathway. Arterioscler Thromb Vasc Biol[J], 2001. 21 (10):
p. 1571-6.
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calmodulin-binding domain of rat cerebellar nitric oxide synthase. J
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calmodulin with its binding domain of rat cerebellar nitric oxide
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Oxide in Changes in Endothelial and Cardiac Function and Biomarker
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2019. 16 (19).
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muscle during hypertension and metabolic disorders.Microcirculation[J], 2018. 25 (1).
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smooth muscle tone. Microcirculation[J], 2018. 25 (1).
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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.