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Expression of catechol-O-methyltransferase (Comt), mineralocorticoid receptor (Mlr), and epithelial sodium channel (ENaC) genes in kidneys of hypertensive ISIAH rats at rest and during response to stress

  • Animal Genetics
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Abstract

Emotional stress plays a significant role in the processes of the development of arterial hypertension, especially in the presence of genetic predisposition. The origin and maintenance of hypertensive status during stress development can be activated by the sympathetic nervous system. An increase in sympathetic stimulation can, in turn, result in a change in the functions of kidneys, which provide fluid and electrolyte balance of the organism. A comparative study of the mRNA expression level of catechol-o-methyltransferase (Comt), mineralocorticoid receptor (Mlr), and β-subunit of epithelial sodium channel (β-ENaC) genes was conducted on the kidneys of hypertensive ISIAH rats and normotensive WAG rats at rest and after the effect of emotional stress. The discovered changes in the expression level of the selected genes confirm their involvement in increased sympathetic stimulation of the kidney, along with changes in the function of kidney regulation of fluid and electrolyte balance, which is an important factor of the development of sustained hypertension in the ISIAH rats strain.

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References

  1. Markel, A.L., Evolutionary and genetic roots of hypertensive disease, Russ. J. Genet., 2015, vol. 51, no. 6, pp. 545–557.

    Article  CAS  Google Scholar 

  2. Laragh, J.H., The renin system and four lines of hypertension research, Hypertension, 1992, vol. 20, no. 3, pp. 267–279.

    Article  CAS  PubMed  Google Scholar 

  3. Paton, J.F.R. and Raizada, M.K., Neurogenic hypertension, Exp. Physiol., 2010, vol. 95, no. 5, pp. 569–571.

    Article  PubMed  Google Scholar 

  4. Markel, A.L., Development of a new strain of rats with inherited stress-induced arterial hypertension, in Genetic Hypertension, Sassard, J., Ed., London: Colloque INSERM, 1992, pp. 405–407.

    Google Scholar 

  5. Markel, A.L., Maslova, L.N., Shishkina, G.T., et al., Developmental influences on blood pressure regulation in ISIAH rat, Development of the Hypertensive Phenotype: Basic and Clinical Studies, Amsterdam: Elsevier, 1999, pp. 405–407.

    Google Scholar 

  6. Markel, A.L., Redina, O.E., Gilinsky, M.A., et al., Neuroendocrine profiling in inherited stress-induced arterial hypertension rat strain with stress-sensitive arterial hypertension, J. Endocrinol., 2007, vol. 195, no. 3, pp. 439–450.

    Article  CAS  PubMed  Google Scholar 

  7. Shmerling, M.D., Filyushina, E.E., Lazarev, V.A., et al., Ultrastructural changes of kidney corpuscles in rats with hereditary stress-induced arterial hypertension, Morphology (Rus), 2001, vol. 120, no. 3, pp. 70–74.

    CAS  Google Scholar 

  8. Filyushina, E.E., Shmerling, M.D., Lazarev, V.A., et al., Structural characteristics of renal glomerular system in ISIAH rats under conditions of chronic stress at the background of preventive administration of antihypertensive drugs, Bull. Exp. Biol. Med. (Rus), 2011, vol. 152, no. 4, pp. 211–214.

    Google Scholar 

  9. Pyl’nik, T.O., Redina, O.E., Smolenskaya, S.E., et al., Specifics of expression of the genes Egf and Egfr in renal tissue of the hypertensive ISIAH rats, Ross. Physiol. Zh. im. I.M. Sechenova, 2012, vol. 98, no. 3, pp. 69–76.

    Google Scholar 

  10. Abramova, T.O., Redina, O.E., Smolenskaya, S.E., et al., Elevated expression of the Ephx2 mRNA in the kidney of hypertensive ISIAH rats, Mol. Biol. (Moscow), 2013, vol. 47, no. 6, pp. 821–826.

    Article  CAS  Google Scholar 

  11. Kiryluk, K., Jadoon, A., Gupta, M., et al., Sickle cell trait and gross hematuria, Kidney Int. Suppl., 2007, vol. 71, no. 7, pp. 706–710.

    Article  CAS  Google Scholar 

  12. Hirano, Y., Tsunoda, M., Shimosawa, T., et al., Suppression of catechol-O-methyltransferase activity through blunting of alpha2-adrenoceptor can explain hypertension in Dahl salt-sensitive rats, Hypertens. Res., 2007, vol. 30, no. 3, pp. 269–278.

    Article  CAS  PubMed  Google Scholar 

  13. Nagase, M., Matsui, H., Shibata, S., et al., Saltinduced nephropathy in obese spontaneously hypertensive rats via paradoxical activation of the mineralocorticoid receptor: role of oxidative stress, Hypertension, 2007, vol. 50, no. 5, pp. 877–883.

    Article  CAS  PubMed  Google Scholar 

  14. Gao, L., Wang, L., Liu, Y., et al., A family with Liddle syndrome caused by a novel missense mutation in the PY motif of the beta-subunit of the epithelial sodium channel, J. Peditr., 2012, vol. 162, no. 1, pp. 166–170.

    Article  Google Scholar 

  15. Mannisto, P.T. and Kaakkola, S., Catechol-O-methyltransferase (COMT): biochemistry, molecular biology, pharmacology, and clinical efficacy of the new selective COMT inhibitors, Pharmacol. Rev., 1999, vol. 51, no. 4, pp. 593–628.

    CAS  PubMed  Google Scholar 

  16. Kajimoto, K., Hiura, Y., Sumiya, T., et al., Exclusion of the catechol-O-methyltransferase gene from genes contributing to salt-sensitive hypertension in Dahl saltsensitive rats, Hypertens. Res., 2007, vol. 30, no. 5, pp. 459–467.

    Article  CAS  PubMed  Google Scholar 

  17. Tsunoda, M., Role of catecholamine metabolism in blood pressure regulation using chemiluminescence reaction detection, Yakugaku Zasshi, 2008, vol. 128, no. 11, pp. 1589–1594.

    Article  PubMed  Google Scholar 

  18. Eklof, A.C., Holtback, U., Sundelof, M., et al., Inhibition of COMT induces dopamine-dependent natriuresis and inhibition of proximal tubular Na+, K+-ATPase, Kidney Int., 1997, vol. 52, no. 3, pp. 742–747.

    Article  CAS  PubMed  Google Scholar 

  19. Carey, R.M., Theodore Cooper lecture: renal dopamine system: paracrine regulator of sodium homeostasis and blood pressure, Hypertension, 2001, vol. 38, no. 3, pp. 297–302.

    Article  CAS  PubMed  Google Scholar 

  20. DiBona, G.F., Zambraski, E.J., Aguilera, A.J., et al., Neurogenic control of renal tubular sodium reabsorption in the dog: a brief review and preliminary report concerning possible humoral mediation, Circ. Res., 1977, vol. 40, suppl. 1, pp. 127–130.

    Google Scholar 

  21. Ryazanova, M.A., Alfa1a adrenoreceptor and alpha2a adrenoreceptor genes expression in myocardium and kidney tissue in hypertensive ISIAH rats, Byull. Sib. Otd. Ross. Akad. Med. Nauk, 2012, vol. 32, no. 1, pp. 43–47.

    Google Scholar 

  22. Fedoseeva, L.A., Ryazanova, M.A., Antonov, E.V., et al., Gene expression of renin kidney system and heart in hypertensive NISAG rats, Biomed. Khim., 2011, vol. 57, no. 4, pp. 410–419.

    Article  CAS  PubMed  Google Scholar 

  23. DiBona, G.F., Sympathetic nervous system and the kidney in hypertension, Curr. Opin. Nephrol. Hypertens., 2002, vol. 11, no. 2, pp. 197–200.

    Article  PubMed  Google Scholar 

  24. Grassi, G., Bertoli, S., and Seravalle, G., Sympathetic nervous system: role in hypertension and in chronic kidney disease, Curr. Opin. Nephrol. Hypertens., 2012, vol. 21, no. 1, pp. 46–51.

    Article  CAS  PubMed  Google Scholar 

  25. Pyl’nik, T.O., Pletneva, L.S., Redina, O.E., et al., The effect of emotional stress on the expression of the a-ENaC gene mRNA in the kidney of hypertensive ISIAH rats, Dokl. Biol. Sci., 2011, vol. 439, no. 4, pp. 201–203.

    Article  Google Scholar 

  26. Kawarazaki, H., Katsuyuki, A., Shigeru, S., et al., Mineralocorticoid receptor-Rac1 activation and oxidative stress play major roles in salt-induced hypertension and kidney injury in prepubertal rats, J. Hypertens., 2012, vol. 30, no. 10, pp. 1977–1985.

    Article  CAS  PubMed  Google Scholar 

  27. White, P.C., Mune, T., and Agarwal, A.K., 11Betahydroxysteroid dehydrogenase and the syndrome of apparent mineralocorticoid excess, Endocr. Rev., 1997, vol. 18, no. 1, pp. 135–156.

    CAS  PubMed  Google Scholar 

  28. Bostanjoglo, M., Reeves, W.B., Reilly, R.F., et al., 11Beta-hydroxysteroid dehydrogenase, mineralocorticoid receptor, and thiazide-sensitive Na–Cl cotransporter expression by distal tubules, J. Am. Soc. Nephrol., 1998, vol. 9, no. 8, pp. 1347–1358.

    CAS  PubMed  Google Scholar 

  29. Gomez-Sanchez, E.P., Romero, D.G., de Rodriguez, A.F., et al., Hexose-6-phosphate dehydrogenase and 11betahydroxysteroid dehydrogenase-1 tissue distribution in the rat, Endocrinology, 2008, vol. 149, no. 2, pp. 525–533.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  30. Gong, R., Latif, S., Morris, D.J., et al., Co-localization of glucocorticoid metabolizing and prostaglandin synthesizing enzymes in rat kidney and liver, Life Sci., 2008, vol. 83, nos. 21–22, pp. 725–731.

    Article  CAS  PubMed  Google Scholar 

  31. Gomez-Sanchez, E. and Gomez-Sanchez, C.E., The multifaceted mineralocorticoid receptor, Compr. Physiol., 2014, vol. 4, no. 3, pp. 965–994.

    Article  PubMed  PubMed Central  Google Scholar 

  32. Odermatt, A. and Kratschmar, D.V., Mineralocorticoids and the mineralocorticoid receptor tißsue-specific modulation of mineralocorticoid receptor function by 11ß-hydroxysteroid dehydrogenases, Mol. Cell. Endocrinol., 2012, vol. 350, no. 2, pp. 168–186.

    Article  CAS  PubMed  Google Scholar 

  33. Cherkasova, O.P., Activity of liver and kidneys 11hydroxysteroid dehydrogenase of rats under stress induced hereditary arterial hypertension, Biomed. Khim., 2006, vol. 52, no. 6, pp. 568–575.

    CAS  PubMed  Google Scholar 

  34. Kim, S.W., Wang, W., Kwon, T.H., et al., Increased expression of ENaC subunits and increased apical targeting of AQP2 in the kidneys of spontaneously hypertensive rats, Am. J. Physiol. Renal Physiol., 2005, vol. 289, no. 5, pp. 957–968.

    Article  Google Scholar 

  35. Amin, M.S., Reza, E., El-Shahat, E., et al., Enhanced expression of epithelial sodium channels in the renal medulla of Dahl S rats, Can. J. Physiol. Pharmacol., 2011, vol. 89, no. 3, pp. 159–168.

    Article  CAS  PubMed  Google Scholar 

  36. Falin, R.A. and Cotton, C.U., Acute downregulation of ENaC by EGF involves the P Ymotif and putative ERK phosphorylation site, J. Gen. Physiol., 2007, vol. 130, no. 3, pp. 313–328.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  37. Touyz, R.M., Reactive oxygen species in vascular biology: role in arterial hypertension, Expert Rev. Cardiovasc. Ther., 2003, vol. 1, pp. 91–106.

    Article  CAS  PubMed  Google Scholar 

  38. Ying, W. and Sanders, W., Enhanced expression of EGF receptor in a model of salt-sensitive hypertension, Am. J. Physiol. Renal Physiol., 2005, vol. 289, pp. 314–321.

    Article  Google Scholar 

  39. Zhang, Z., Hu, D., and Zhou, M., 14,15-Epoxyeicosatrienoic acid induces the proliferation and anti-apoptosis of human carcinoma cell, Daru, 2011, vol. 19, no. 6, pp. 462–468.

    CAS  PubMed  PubMed Central  Google Scholar 

  40. Esler, M., The sympathetic system and hypertension, Am. J. Hypertens., 2000, vol. 13, no. 6, part 2, pp. 99–105.

    Article  Google Scholar 

  41. Guyton, A.C., Manning, R.D., and Hall, J.E., The pathogenic role of the kidney, J. Cardiovasc. Pharmacol., 1984, vol. 846, no. 6, suppl., pp. 151–161.

    Article  Google Scholar 

  42. Kurokawa, K., Kidney, salt, and hypertension: how and why, Kidney Int. Suppl., 1996, vol. 55, pp. 46–51.

    Google Scholar 

  43. Brenner, B.M. and Mackenzie, H.S., Nephron mass as a risk factor for progression of renal disease, Kidney Int. Suppl., 1997, vol. 63, pp. 124–127.

    Google Scholar 

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Correspondence to T. O. Abramova.

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Original Russian Text © T.O. Abramova, S.E. Smolenskaya, E.V. Antonov, O.E. Redina, A.L. Markel, 2016, published in Genetika, 2016, Vol. 52, No. 2, pp. 206–214.

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Abramova, T.O., Smolenskaya, S.E., Antonov, E.V. et al. Expression of catechol-O-methyltransferase (Comt), mineralocorticoid receptor (Mlr), and epithelial sodium channel (ENaC) genes in kidneys of hypertensive ISIAH rats at rest and during response to stress. Russ J Genet 52, 180–187 (2016). https://doi.org/10.1134/S1022795415120029

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