Endothelium-dependent hyperpolarization-mediated relaxation pathway in bovine mesenteric lymph nodes
- Authors: Lobov G.I.1, Dvoretskii D.P.1
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Affiliations:
- Pavlov Institute of Physiology of the Russian Academy of Sciences
- Issue: Vol 484, No 5 (2019)
- Pages: 645-648
- Section: Physiology
- URL: https://journals.eco-vector.com/0869-5652/article/view/12793
- DOI: https://doi.org/10.31857/S0869-56524845645-648
- ID: 12793
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Abstract
In vitro, endothelium-dependent relaxation mechanisms of smooth muscle cells of the bovine mesenteric lymph node capsule have been studied. The addition of L-NAME and indomethacin to physiological saline inhibited the production of endothelium NO and prostacyclin. In this solution, tetraethylammonium chloride and TRAM-34 increased the tone of the precontracted lymph nodes. Thus, in bovine mesenteric lymph nodes there is an relaxation mechanism mediated by endothelial hyperpolarization, realized by activating Ca2+-dependent K+-channels of large- and intermediate conductance.
About the authors
G. I. Lobov
Pavlov Institute of Physiology of the Russian Academy of Sciences
Author for correspondence.
Email: gilobov@yandex.ru
Russian Federation, Saint-Petersburg
D. P. Dvoretskii
Pavlov Institute of Physiology of the Russian Academy of Sciences
Email: gilobov@yandex.ru
Corresponding Member of the RAS
Russian Federation, Saint-PetersburgReferences
- Лобов Г.И., Панькова М.Н. // Рос. физиол. журн. им. И.М. Сеченова. ٢٠١٢. Т. ٩٨. № ١١. С. ١٣٥٠–1361.
- Унт Д.В., Лобов Г.И. // Бюл. экспер. биологии и медицины. 2017. Т. 164. № 8. С. 145–149.
- Brandes R.P., Schmitz-Winnenthal F.H., Félétou M., et al. // Proc. Natl. Acad. Sci. USA. 2000. V. 97. № 17. P. 9747–9752.
- Furchgott R.F., Zawadzki J.V. // Nature. 1980. V. 288. № 5789. Р. 373–376.
- Furchgott R.F., Cherry P.D., Zawadzki J.V., Jothianandan D. // J. Cardiovasc. Pharmacol. 1984. V. 6. Suppl. 2. Р. S 336–S343.
- Hurjui L., Serban. I.L., Oprişa C., et al. // Rev. Med. Chir. Soc. Med. Nat. Iasi. 2011. V. 115. № 1. P. 168–170.
- Jin X., Satoh-Otonashi Y., Zamami Y., et al. // J. Pharmacol. Sci. 2011. V. 116. № 4. P. 332–336.
- Kobuchi S., Miura K., Iwao H., Ayajiki K. // Eur. J. Pharmacol. 2015. V. 762. P. 26–34.
- Liu Z.G., Ge Z.D., He G. W. // Circulation. 2000. V. 102. № 19. Suppl. 3. P. 296–301.
- Nishikawa Y., Stepp D.W., Chilian W.M. // Amer. J. Physiol. Heart Circ. Physiol. 2000. V. 279. № 2. P. H459–H465.
- Reeder L.B., Yang L.H., Ferguson M.K. // J. Surg. Res. 1994. V. 56. № 6. P. 620–625.
- Shimokawa H., Yasutake H., Fujii K.J., et al. // Cardiovasc. Pharmacol. 1996. V. 28 P. 703–711.
- Vanhoutte P.M., Shimokawa H., Tang E.H., Félétou M. // Acta Physiol. 2009. V. 196. № 2. P. 193–222.
- Yokoyama S., Ohhashi T. // Amer. J. Physiol. 1993. V. 264. № 5. Pt 2. P. H1460–H1464.
- Zhang R.Z., Yang Q., Yim A.P., et al. // Vascul. Pharmacol. 2006. V. 44. № 3. P. 183–191.