Plasma Concentrations of 6-Keto-Prostaglandin F1α, Thromboxane B2 and Platelet Aggregation in Patients with Essential Hypertension

Long Shiung CHEN; Takayuki ITO; Kouichi OGAWA; Masahiko SHIKANO; Tatsuo SATAKE

doi:10.1536/ihj.25.1001

Plasma Concentrations of 6-Keto-Prostaglandin F_1α, Thromboxane B₂ and Platelet Aggregation in Patients with Essential Hypertension

Long Shiung CHEN, Takayuki ITO, Kouichi OGAWA, Masahiko SHIKANO, Tatsuo SATAKE

著者情報

キーワード: Prostacyclin, Thromboxane A₂, Tourniquet test

ジャーナルフリー

1984 年 25 巻 6 号 p. 1001-1009

DOI https://doi.org/10.1536/ihj.25.1001

詳細

Published: 1984 Received: 1983/09/28 Available on J-STAGE: 2008/12/09 Accepted: - Advance online publication: - Revised: -
訂正情報
訂正日: 2008/12/09 訂正理由: - 訂正箇所: 論文タイトル訂正内容: Wrong : Plasma Concentrations of 6-Keto-Prostaglandin F_1α, Thromboxane B₂ and Platelet Aggregation in Patients with Essential Hypertension
Right : Plasma Concentrations of 6-Keto-Prostaglandin F_1α, Thromboxane B₂ and Platelet Aggregation in Patients with Essential Hypertension

訂正日: 2008/12/09 訂正理由: - 訂正箇所: 論文抄録訂正内容: Wrong : Plasma concentrations of 6-keto-prostaglandin F_1α (6-keto-PGF_1α) and thromboxane B₂ (TXB₂), the stable nonenzymatic metabolites of prostacyclin and TXA₂, respectively, were assayed in 26 patients with essential hypertension and 25 normotensive subjects to investigate the pathophysiological role of prostacyclin and thromboxane A₂ (TXA₂) in essential hypertension. A tourniquet test was also performed on the upper limb of each subject to study the reactivity in peripheral vessels. In addition, platelet aggregation was investigated.
There were significantly increased plasma TXB₂ concentrations and platelet aggregation and significantly decreased plasma 6-keto-PGF_1α concentrations in patients with essential hypertension as compared with normotensive subjects. The responses to tourniquet tests were also different. There were significantly increased plasma concentrations of 6-keto-PGF_1α and TXB₂ and platelet aggregation in normotensive subjects, but no significant changes with essential hypertension as compared to resting values.
These results indicate that the reduction of plasma prostacyclin and increase of plasma TXA₂ may contribute to the maintenance of blood pressure elevation in patients with essential hypertension. In addition, it is also suggested that increased prostacyclin generation in normotensive subjects during the tourniquet test is a protective mechanism. In patients with essential hypertension, the protective activity is reduced.
Right : Plasma concentrations of 6-keto-prostaglandin F_1α (6-keto-PGF_1α) and thromboxane B₂ (TXB₂), the stable nonenzymatic metabolites of prostacyclin and TXA₂, respectively, were assayed in 26 patients with essential hypertension and 25 normotensive subjects to investigate the pathophysiological role of prostacyclin and thromboxane A₂ (TXA₂) in essential hypertension. A tourniquet test was also performed on the upper limb of each subject to study the reactivity in peripheral vessels. In addition, platelet aggregation was investigated.
There were significantly increased plasma TXB₂ concentrations and platelet aggregation and significantly decreased plasma 6-keto-PGF_1α concentrations in patients with essential hypertension as compared with normotensive subjects. The responses to tourniquet tests were also different. There were significantly increased plasma concentrations of 6-keto-PGF_1α and TXB₂ and platelet aggregation in normotensive subjects, but no significant changes with essential hypertension as compared to resting values.
These results indicate that the reduction of plasma prostacyclin and increase of plasma TXA₂ may contribute to the maintenance of blood pressure elevation in patients with essential hypertension. In addition, it is also suggested that increased prostacyclin generation in normotensive subjects during the tourniquet test is a protective mechanism. In patients with essential hypertension, the protective activity is reduced.

訂正日: 2008/12/09 訂正理由: - 訂正箇所: 所属機関情報訂正内容: 訂正前 :
1) Second Department of Internal Medicine, Nagoya University School of Medicine

訂正後 :
1) the Second Department of Internal Medicine, Nagoya University School of Medicine

訂正日: 2008/12/09 訂正理由: - 訂正箇所: キーワード情報訂正内容: Wrong : Prostacyclin, Thromboxane A₂, Tourniquet test
Right : Prostacyclin, Thromboxane A₂, Tourniquet test

訂正日: 2008/12/09 訂正理由: - 訂正箇所: 引用文献情報訂正内容: Wrong : 1. Born GVR: Aggregation of platelets by ADP and its reversal. Nature 194: 927, 1962
2. Hennam JF, Tohnsonm DA, Newton JR, Cillins WP: Radioimmunoassay of prostaglandin F_2α in peripheral venous plasma from men and women. Prostaglandin 5: 531, 1974
3. Caldwell BV, Burstein S, Brock WA, Speroff L: Radioimmunoassay of the F prostaglandins. J Clin Endocr 33: 171, 1971
4. Dembinska-Kiec A, Gryglewska T, Zmuda A, Gryglwski RJ: The generation of prostacyclin by arteries and by the coronary vascular bed is reduced in experimental atherosclerosis in rabbits. Prostaglandins 14: 1025, 1977
5. Chen LS, Ito T, Ogawa K, Satake T: Changes of plasma 6-keto-PGF_1α and thromboxane B₂ levels and platelet aggregation after tourniquet ischemia on the upper limb in normal subjects and patients with ischemic heart disease. Jpn Circulat J 46: 651, 1982
6. Uehara Y, Ishii M, Ikeda T, Atarashi K, Takeda T, Murao S: Plasma levels of 6-keto-prostaglandin F_1α in normotensive subjects and patients with essential hypertension. Prostaglandins, Leukotrienes and Medicine 11: 95, 1983
7. Grose JH, Lebel M, Gbeassor FM: Variations in urinary metabolites of prostacyclin and thromboxane A₂ in essential hypertension. Clin Res 28: 685A, 1980
8. Okuma M, Yamori Y, Ohta K, Uchino H: Production of prostacyclin-like substance in stroke-prone and stroke-resistant spontaneously hypertensive rats. Prostaglandins 17: 1, 1979
9. Roy L, Mehta J, Mehta P, Ostrowski H, Horalek C, Kelley G: Increased plasma concentrations of prostacyclin metabolite 6-keto-PGF1α in essential hypertension. Am J Cardiol 51: 464, 1983
10. Neri Serneri GC, Massotti G, Poggesi L, Galanti G: Release of prostacyclin into the bloodstream in humans after local blood flow changes. Advances in Prostaglandin and Thromboxane Research 7: 715, 1980
11. Vlachakis ND, Aledort FL: Hypertension and propranolol therapy. Effect on blood pressure, plasma catecholamines and platelet aggregation. Am J Cardiol 45: 321, 1980
12. Mehta J, Mehta P: Platelet function in hypertension and effect of therapy. Am J Cardiol 47: 331, 1981
13. Hornych A, Safar M, Simon A, Bariety J: Thromboxane B2 in borderline and essential hypertension. Advances in Prostaglandin, Thromboxane, and Leukotriene Research 11: 417, 1983

Right : 1. Born GVR: Aggregation of platelets by ADP and its reversal. Nature 194: 927, 1962
2. Hennam JF, Tohnsonm DA, Newton JR, Cillins WP: Radioimmunoassay of prostaglandin F_2α in peripheral venous plasma from men and women. Prostaglandin 5: 531, 1974
3. Caldwell BV, Burstein S, Brock WA, Speroff L: Radioimmunoassay of the F prostaglandins. J Clin Endocr 33: 171, 1971
4. Dembinska-Kiec A, Gryglewska T, Zmuda A, Gryglwski RJ: The generation of prostacyclin by arteries and by the coronary vascular bed is reduced in experimental atherosclerosis in rabbits. Prostaglandins 14: 1025, 1977
5. Chen LS, Ito T, Ogawa K, Satake T: Changes of plasma 6-keto-PGF_1α and thromboxane B₂ levels and platelet aggregation after tourniquet ischemia on the upper limb in normal subjects and patients with ischemic heart disease. Jpn Circulat J 46: 651, 1982
6. Uehara Y, Ishii M, Ikeda T, Atarashi K, Takeda T, Murao S: Plasma levels of 6-keto-prostaglandin F_1α in normotensive subjects and patients with essential hypertension. Prostaglandins, Leukotrienes and Medicine 11: 95, 1983
7. Grose JH, Lebel M, Gbeassor FM: Variations in urinary metabolites of prostacyclin and thromboxane A₂ in essential hypertension. Clin Res 28: 685A, 1980
8. Okuma M, Yamori Y, Ohta K, Uchino H: Production of prostacyclin-like substance in stroke-prone and stroke-resistant spontaneously hypertensive rats. Prostaglandins 17: 1, 1979
9. Roy L, Mehta J, Mehta P, Ostrowski H, Horalek C, Kelley G: Increased plasma concentrations of prostacyclin metabolite 6-keto-PGF_1α in essential hypertension. Am J Cardiol 51: 464, 1983
10. Neri Serneri GC, Massotti G, Poggesi L, Galanti G: Release of prostacyclin into the bloodstream in humans after local blood flow changes. Advances in Prostaglandin and Thromboxane Research 7: 715, 1980
11. Vlachakis ND, Aledort FL: Hypertension and propranolol therapy. Effect on blood pressure, plasma catecholamines and platelet aggregation. Am J Cardiol 45: 321, 1980
12. Mehta J, Mehta P: Platelet function in hypertension and effect of therapy. Am J Cardiol 47: 331, 1981
13. Hornych A, Safar M, Simon A, Bariety J: Thromboxane B₂ in borderline and essential hypertension. Advances in Prostaglandin, Thromboxane, and Leukotriene Research 11: 417, 1983

訂正日: 2008/12/09 訂正理由: - 訂正箇所: PDFファイル訂正内容: -

抄録

Plasma concentrations of 6-keto-prostaglandin F_1α (6-keto-PGF_1α) and thromboxane B₂ (TXB₂), the stable nonenzymatic metabolites of prostacyclin and TXA₂, respectively, were assayed in 26 patients with essential hypertension and 25 normotensive subjects to investigate the pathophysiological role of prostacyclin and thromboxane A₂ (TXA₂) in essential hypertension. A tourniquet test was also performed on the upper limb of each subject to study the reactivity in peripheral vessels. In addition, platelet aggregation was investigated.
There were significantly increased plasma TXB₂ concentrations and platelet aggregation and significantly decreased plasma 6-keto-PGF_1α concentrations in patients with essential hypertension as compared with normotensive subjects. The responses to tourniquet tests were also different. There were significantly increased plasma concentrations of 6-keto-PGF_1α and TXB₂ and platelet aggregation in normotensive subjects, but no significant changes with essential hypertension as compared to resting values.
These results indicate that the reduction of plasma prostacyclin and increase of plasma TXA₂ may contribute to the maintenance of blood pressure elevation in patients with essential hypertension. In addition, it is also suggested that increased prostacyclin generation in normotensive subjects during the tourniquet test is a protective mechanism. In patients with essential hypertension, the protective activity is reduced.

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