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.
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