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Unilateral Chronic Ischemia of the Carotid Bodies Alters Sympathetic Nervous System Activity

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Abstract

As is well known, activation of carotid body chemoreceptors that sense arterial blood oxygen can lead to sympathetic nervous system (SNS) activation, while chronic hypoxia-induced activation of the carotid bodies promotes the development of various cardiovascular diseases. It has been shown in the literature that bilateral activation of the carotid bodies reduces chronotropic baroreflex sensitivity, which is restored following their subsequent bilateral ablation. In this work, we demonstrate that unilateral chronic ischemization of the rat carotid bodies by ligation of the external carotid artery decreases chronotropic baroreflex sensitivity, whereas unilateral ablation of the carotid bodies, on the contrary, increases it. At the systemic level, the reduction in SNS activity is further confirmed by a decrease in the glucose level. Our results show that even unilateral hyperactivation or inactivation of the carotid bodies induce systemic alterations in SNS activity.

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REFERENCES

  1. Del Rio R, Andrade DC, Lucero C, Arias P, Iturriaga R (2016) Carotid body ablation abrogates hypertension and autonomic alterations induced by intermittent hypoxia in rats. Hypertension 68(2):436-445. https://doi.org/10.1161/HYPERTENSIONAHA.116.07255

    Article  CAS  PubMed  Google Scholar 

  2. Markov MA, Davydova MP, Usachev DU, Lukshin VA, Balakhonova TV, Rodnenkov OV, Martyniuk TV Pulmonary hypertension in patients with hemodynamically significant atherosclerotic lesion of a common carotid artery: new pathophysiological mechanisms of the disease. Systemic Hypertension 17(2):61-64. https://doi.org/10.26442/2075082X.2020.2.200221

  3. Alzahrani AA, Cao LL, Aldossary HS, Nathanael D, Fu J, Ray CJ, Brain KL, Kumar P, Coney AM, Holmes AP (2021) β-Adrenoceptor blockade prevents carotid body hyperactivity and elevated vascular sympathetic nerve density induced by chronic intermittent hypoxia. Pflugers Arch 473(1):37-51. https://doi.org/10.1007/s00424-020-02492-0

    Article  CAS  PubMed  Google Scholar 

  4. Del Rio R, Andrade DC, Marcus NJ, Schultz HD (2015) Selective carotid body ablation in experimental heart failure: a new therapeutic tool to improve cardiorespiratory control. Exp Physiol 100(2):136-142. https://doi.org/10.1113/expphysiol.2014.079566

    Article  PubMed  PubMed Central  Google Scholar 

  5. Sugito K, Tatsumi K, Igari H, Kasahara Y, Tani T, Kimura H, Hayashi F, Kuriyama T (1998) Role of carotid body in pressure response of pulmonary circulation in rats. Respir Physiol 111(3):283-293. https://doi.org/10.1016/S0034-5687(97)00126-6

    Article  CAS  PubMed  Google Scholar 

  6. Davydova MP, Markov MA, Tesakov IP, Safarova NB (2018) Unilateral ischemia of the carotid body zone in rats leads to the development of pulmonary hypertension and changes the activity of the sympathetic nervous system. Collection of materials internat scientific and pract conference Oxygen and free radicals. GrSMU Publ House Belarus, Grodno 40-42. (In Russ).

    Google Scholar 

  7. Bonnet S, Rochefort G, Sutendra G, Archer SL, Haromy A, Webster L, Hashimoto K, Bonnet SN, Michelakis ED (2007) The nuclear factor of activated T cells in pulmonary arterial hypertension can be therapeutically targeted. Proc Natl Acad Sci USA 104(27):11418-11423. https://doi.org/10.1073/pnas.0610467104

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  8. Bullen JW, Tchernyshyov I, Holewinski RJ, DeVine L, Wu F, Venkatraman V, Kass DL, Cole RN, Van Eyk J, Semenza GL (2016) Protein kinase A-dependent phosphorylation stimulates the transcriptional activity of hypoxia-inducible factor 1. Sci Signal 9(430):ra56. https://doi.org/10.1126/scisignal.aaf0583

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  9. Bonnet S, Michelakis ED, Porter CJ, Andrade-Navarro MA, Thébaud B, Bonnet S, Haromy A, Harry G, Moudgil R, McMurtry MS, Weir EK, Archer SL (2006) An abnormal mitochondrial-hypoxia inducible factor-1alpha-Kv channel pathway disrupts oxygen sensing and triggers pulmonary arterial hypertension in fawn hooded rats: similarities to human pulmonary arterial hypertension. Circulation 113(22):2630-2641. https://doi.org/10.1161/CIRCULATIONAHA.105.609008

    Article  CAS  PubMed  Google Scholar 

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Funding

This work was implemented within the Lomonosov Moscow State University program of studying the pathophysiology of pulmonary hypertension.

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The basic idea and experimental design (M.P.D., M.A.M.); data collection (M.A.M.); data processing (M.P.D.); writing and editing a manuscript (M.A.M., M.P.D.).

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Correspondence to M. A. Markov.

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The authors declare that they have neither evident nor potential conflict of interest associated with the publication of this article.

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Translated by A. Polyanovsky

Russian Text © The Author(s), 2022, published in Rossiiskii Fiziologicheskii Zhurnal imeni I.M. Sechenova, 2022, Vol. 108, No. 1, pp. 13–23https://doi.org/10.31857/S0869813922010095.

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Markov, M.A., Davydova, M.P. Unilateral Chronic Ischemia of the Carotid Bodies Alters Sympathetic Nervous System Activity. J Evol Biochem Phys 58, 81–87 (2022). https://doi.org/10.1134/S0022093022010082

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  • DOI: https://doi.org/10.1134/S0022093022010082

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