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Angiotensin inhibition and malignancies: a question of hydration

Journal of Human Hypertension volume 24, page 226 (2010)Cite this article

A considerable literature is growing concerning the subject of the review article by Rosenthal and Gavras published recently in the journal.1 In this excellent review the authors show that cancer cells of various tissues express components of the renin–angiotensin system and that inhibition of the same system can lead to a decrease in the incidence of cancer in the clinical setting. This review is very comprehensive and covers a good deal of the field. However, I would like to provide an alternative, and perhaps more mechanistic, view of angiotensin (AngII) and its relation to cancer. The exact mechanism(s) of the interaction between AngII and cancer is unknown and could occur during the initiation, the development and/or maintenance of either pathology.

Nevertheless, production of the AngII is well understood; its release into the vascular system is in response to a decrease in blood volume, hypovolaemia. A reduction in blood flow through the kidney juxtaglomerular apparatus releases the enzyme renin into the blood, which cleaves the precursor, angiotensinogen, into angiotensin I. Subsequently, the action of lung angiotensin-converting enzyme leads to the formation of AngII. The principal actions of AngII are vasoconstriction, to increase plasma levels of aldosterone (re-absorption of sodium in the kidneys) and to initiate drinking behaviour. Under ideal physiological conditions these actions support cardiovascular regulation, which in reality means maintaining tissue perfusion (supply to the cells of nutriments), and quickly returns blood volume to normal levels. This, in turn, would decrease the release of renin and thus decrease AngII.

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References

  1. Rosenthal T, Gavras I . Angiotensin inhibition and malignancies: a review. J Hum Hypertens 2009; 23: 623–635.

    Article  CAS  Google Scholar 

  2. Thornton SN . Angiotensin, the hypovolaemia hormone, aggravates hypertension, obesity, diabetes and cancer. J Intern Med 2009; 265: 616–617.

    Article  CAS  Google Scholar 

  3. Thornton SN . Angiotensin-induced metabolic dysfunction. J Hypertens 2009; 27: 658–659.

    Article  CAS  Google Scholar 

  4. Thornton SN . Hypovolaemia-induced mild hypoxia produces sub-chronic metabolic dysfunction. Int J Obes (London) 2009; 33: 605.

    Article  CAS  Google Scholar 

  5. Thornton SN, Even PC, van Dijk G . Hydration increases cell metabolism. Int J Obes (London) 2009; 33: 385.

    Article  CAS  Google Scholar 

  6. Sun Y, Eichelbaum EJ, Lenz A, Skelton IV WP, Wang H, Vesely DL . Atrial natriuretic peptide and long-acting natriuretic peptide inhibit ras in human prostate cancer cells. Anticancer Res 2009; 29: 1889–1893.

    CAS  PubMed  Google Scholar 

  7. Kong X, Wang X, Xu W, Behera S, Hellermann G, Kumar A et al. Natriuretic peptide receptor A as a novel anticancer target. Cancer Res 2008; 68: 249–256.

    Article  CAS  Google Scholar 

  8. Thornton SN . Angiotensin, the hormone to be blocked by antithypertensive drugs, and perhaps why they don’t work. Curr Vasc Pharmacol 2009; 7: 549.

    Article  CAS  Google Scholar 

  9. Altieri A, La Vecchia C, Negri E . Fluid intake and risk of bladder and other cancers. Eur J Clin Nutr 2003; 57 (Suppl 2): S59–S68.

    Article  Google Scholar 

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Authors and Affiliations

  1. Université Henri Poincaré, Nancy Université, Nancy, France

    S N Thornton

  2. INSERM, U961, Vandoeuvre les Nancy, France

    S N Thornton

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  1. S N Thornton
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Correspondence to S N Thornton.

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Thornton, S. Angiotensin inhibition and malignancies: a question of hydration. J Hum Hypertens 24, 226 (2010). https://doi.org/10.1038/jhh.2009.111

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