Response to Prof. Tsuda Letter

American Journal of Hypertension, Aug 2006

Papadopoulos, Dimitris P.

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Response to Prof. Tsuda Letter

AJH–August 2006 –VOL. 19, NO. 8 7. Nakata M, Yada T, Soejima N, Maruyama I: Leptin promotes aggregation of human platelets via the long form of its receptor. Diabetes 1999;48:426 – 429. 8. Konstantinou-Tegou A, Kaloyianni M, Bourikas D, Koliakos G: The effect of leptin on Na ⫹-H⫹ antiport (NHE 1) activity of obese and normal subjects erythrocytes. Mol Cell Endocrinol 2001;183: 11–18. 9. Tsuda K, Kimura K, Nishio I: Leptin improves membrane fluidity of erythrocytes in humans via a nitric oxide-dependent mechanism —an electron paramagnetic resonance investigation. Biochem Biophys Res Commun 2002;297:672– 681. 10. Kimura K, Tsuda K, Baba A, Kawabe T, Boh-oka S, Ibata M, Moriwaki C, Hano T, Nishio I: Involvement of nitric oxide in endothelium-dependent arterial relaxation by leptin. Biochem Biophys Res Commun 2000;273:745–749. 11. Tsuda K, Nishio I: Leptin and membrane fluidity of erythrocytes in essential hypertension. Am J Hypertens 2004;17:375–379. Response to Prof. Tsuda Letter To the Editor: We read with great interest in your journal the letter by Professor Tsuda1 dealing the relation of leptin receptor and membrane microviscosity of erythrocytes in essential hypertension. Its is well known from literature data that the cause– effect relationship between leptin and essential hypertension in human beings has not been demonstrated directly, although many clinical studies have shown elevated plasma leptin in patients with essential hypertension and a significant positive correlation between leptin and blood pressure independent of body adiposity, both in normotensive and in hypertensive individuals. In addition, leptin may contribute to end-organ damage such as left ventricular hypertrophy in hypertensive individuals, inde- LETTER TO THE EDITOR 875 pendent of blood pressure regulation.2,3 Finally, our results have demonstrated that normotensive individuals with high-normal blood pressure have significantly elevated leptin plasma levels and significantly decreased numbers of human soluble leptin receptors compared to normotensive individuals. A limitation of our study was that we have not evaluated tissue leptin receptor number, although it is well known that leptin exerts its effect by using tissue receptors, whereas the role of soluble receptors is not completely clarified.4 DIMITRIS P. PAPADOPOULOS Department of Cardiology Laiko Hospital Athens, Greece doi:10.1016/j.amjhyper.2006.05.009 Address correspondence and reprint requests to Dr. Dimitris P. Papadopoulos, Cardiology, Laiko Hospital, 6-8 Glykonos Street, 10675 Athens, Greece; e-mail: References 1. 2. 3. 4. Tsuda K: Leptin receptor and membrane microviscosity of erythrocytes in essential hypertension. Am J Hypertens 2006;19. Beltowski J: Role of leptin in blood pressure regulation and arterial hypertension. J Hypertens 2006;24:789 – 801. Makris TK, Stavroulakis GA, Krespi PG, Hatzizacharias AN, Kyriaki DK, Chronakis EV, Anastasiadis G, Triposkiadis FK, Kyriakidis MK: Elevated plasma immunoreactive leptin levels preexist in healthy offspring of patients with essential hypertension. Am Heart J 1999;138:922–925. Papadopoulos DP, Makris TA, Krespi PG, Poulakou M, Paizis IA, Hatzizacharias AN, Perrea D, Votteas VV: Human soluble leptin receptor number in healthy normotensive individuals with high normal blood pressure. Am J Hypertens 2005;18:1001–1004. (...truncated)


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Papadopoulos, Dimitris P.. Response to Prof. Tsuda Letter, American Journal of Hypertension, 2006, pp. 875, Volume 19, Issue 8, DOI: 10.1016/j.amjhyper.2006.05.009