Volume 3 Issue 7 - 2021
Immunity Participation in the Hypertension Pathology
Irene Burguillo Diez*
Director of Nursing and Clinical Services, CODEM, Spain and Clinical Nurse Specialist, NMC, UK
*Corresponding Author: Irene Burguillo Diez, Director of Nursing and Clinical Services, CODEM, Spain and Clinical Nurse Specialist, NMC, UK.
Received: October 21, 2020; Published: June 28, 2021

Research that have led to immune system participation in the pathology of Hypertension are relatively new.

Association between HTA and renal disease was reported on 1879 [2] and the first description of autoimmunity as producing morbid situation appeared on 1904 when the antibodies description causing hemolytic anemia in the crio hemoglobin paroxysmic [2] where the end of the stated situation by Paul Erlich who established that the organism didn’t hurt himself (horror autotoxicus) [3].


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    4. Svendsen UG. “Studies elucidating the importance of thymus on the degree of increased blood pressure and vascular disease in renal hypertensive mice. A comparison of the disease in nude and haired littermates”. Journals Acta pathologica et microbiologica Scandinavica. Section A 83 (1975): 568-572.
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    6. Norlander AE., et al. “The immunology of hypertension”. Journal of Experimental Medicine 215 (2018): 21-33.
    7. Rodriguez-Iturbe B., et al. “Role of the immune system in hypertension”. Physiological Reviews 97 (2017): 1127-1164.
    8. Abais-Battad JM., et al. “Novel adaptive and innate immunity targets in hypertension”. Pharmacological Research 120 (2017): 109-115.
    9. Guyton AC., et al. “Arterial pressure regulation overriding dominance of the kidneys in long-term regulation and in hypertension”. The American Journal of Medicine 52 (1972): 584-594.
    10. Guzik TJ., et al. “Role of the T cell in the genesis of angiotensin II induced hypertension and vascular dysfunction”. Journal of Experimental Medicine 204 (2007): 2449-2460.
    11. Mattson DL., et al. “Genetic mutation of recombination activating gene 1 in Dahl salt-sensitive rats attenuates hypertension and renal damage”. The American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 304 (2013): R407-R414.
    12. Chan CT., et al. “Obligatory role for B cells in the development of angiotensin II-dependent hypertension”. Hypertension 66 (2015): 1023-1033.
    13. Liu D., et al. “Role of NLRP3 inflammasome in the pathogenesis of cardiovascular diseases”. Basic Research in Cardiology 113 (2017): 5.
    14. Marketou ME., et al. “TLR2 and TLR4 gene expression in peripheral monocytes in nondiabetic hypertensive patients: The effect of intensive blood pressure-lowering”. Journal of Clinical Hypertension 14 (2012): 330-335.
    15. Zirlik A., et al. “Interleukin-18, the metabolic syndrome, and subclinical atherosclerosis: Results from the Dallas Heart Study”. Arteriosclerosis, Thrombosis, and Vascular Biology 27 (2007): 2043-2049.
    16. Blankenberg S., et al. “PRIME Study Group Interleukin-18 and the risk of coronary heart disease in European men: The Prospective Epidemiological Study of Myocardial Infarction (PRIME)”. Circulation 108 (2003): 2453-2459.
    17. Kirabo A., et al. “DC isoketal-modified proteins activate T cells and promote hypertension”. Journal of Clinical Investigation 124 (2014): 4642-456.
    18. Vinh A., et al. “Inhibition and genetic ablation of the B7/CD28 T-cell costimulation axis prevents experimental hypertension”. Circulation 122 (2010): 2529-2537.
    19. Itani HA., et al. “CD70 exacerbates blood pressure elevation and renal damage in response to repeated hypertensive stimuli”. Circulation Research 118 (2016): 1233-1243.
    20. Pockley AG., et al. “Circulating heat shock protein and heat shock protein antibody levels in established hypertension”. Journal of Hypertension 20 (2002): 1815-1820.
    21. Wu T., et al. “Association of plasma antibodies against the inducible Hsp70 with hypertension and harsh working conditions”. Cell Stress Chaperones 6 (2001): 394-401.
    22. Wu C., et al. “Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1”. Nature 496 (2013): 513-517.
    23. Kleinewietfeld M., et al. “Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells”. Nature 496 (2013): 518-522.
    24. Norlander AE., et al. “A salt-sensing kinase in T lymphocytes SGK1, drives hypertension and hypertensive end-organ damage”. JCI Insight 2 (2017): e92801.
    25. O’Dounaughy TL and Brooks VL. “Deoxycorticosterone acetate-salt rats: Hypertension and sympathoexcitation driven by increased NaCl levels”. Hypertension 47 (2006): 680-685.
    26. Wiig H., et al. “Immune cells control skin lymphatic electrolyte homeostasis and blood pressure”. Journal of Clinical Investigation 123 (2013): 2803-2815.
    27. Pons H., et al. “Immune reactivity to heat shock protein 70 expressed in the kidney is cause of salt sensitive hypertension”. The American Journal of Physiology-Renal Physiology 304 (2013): F289-F299.
    28. Rodriguez-Iturbe B., et al. “The role of autoimmune reactivity induced by heat shock protein 70 in the pathogenesis of essential hypertension”. British Journal of Pharmacology (2018).
    29. Chen J., et al. “Inflammation and apparent treatment resistant-hypertension in patients with chronic kidney disease: The results from the CRIC study”. Hypertension 73 (2019): 785-793.
    30. Barbaro NR and Harrison DG. “Markers or makers: Inflammatory cytokines in treatment-resistant hypertension”. Hypertension 73 (2019): 767-769.
    31. Rodriguez-Iturbe B. “Autoimmunity in the pathogenesis of hypertension”. Hypertension 67 (2016): 477-483.
Citation: Irene Burguillo Diez. “Immunity Participation in the Hypertension Pathology”. EC Nursing and Healthcare 3.7 (2021): 11-15.

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