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12. Role of prostaglandin H2 as an endothelium-derived contracting factor in diabetic state

Author

Shimizu, Kiyokazu, Muramatsu, Masahito, Kakegawa, Yoshio, Asano, Hiroshi, Toki, Yukio, Miyazaki, Yutaka, Okumura, Kenji, Hashimoto, Hidekazu, and Ito, Takayuki

Subjects
Prostaglandins -- Physiological aspects, Diabetic angiopathies -- Development and progression, Health, Physiological aspects, Development and progression
Abstract

This study investigated the possible involvement of prostaglandin [H.sub.2], an acetylcholine-induced ondothelium-derived contracting factor in rat aorta, in the development of abnormality of the vasculature in diabetes. Rings of thoracic aorta were prepared from control Wistar-Kyoto and STZ-induced diabetic rats to examine the changes in isometric tension. In [10.sup.-7] M norepinephrine-precontracted rings, acetylcholine induced relaxations, which were significantly impaired in diabetic rats. Inhibition of thromboxane [A.sub.2]-prostaglandin [H.sub.2] receptors with ONO-3708 ([10.sup.-6] m) prevented the development of the impairment of relaxation in diabetic rats. Thromboxane [A.sub.2] synthesis inhibition with OKY-046 ([10.sup.-5] m) did not affect the acetylcholine-induced relaxation in both control and diabetic rats. In aortic rings under resting tension, acetylcholine induced a contraction that was greater in diabetic than control rate, when the nitric oxide production was inhibited by [N.sup.g]-nitro-L-arginine methylester ([10.sup.-4] M). This acetylcholine-induced contraction was observed only in the rings with intact endathelium and was completely abolished by ONO-3708 ([10.sup.-6] M). The concentration of 6-keto-prostaglandin [F.sub.alpha] in the solution bathing diabetic rat aortic rings increased significantly after acetylcholine ([10.sup.-15] M) administration. Prostacyclin ([10.sup.-9]-[10.sup.-6] M) did not induce contractions at all. Prostacyclin is unlikely to mediate contractions because of its low contractile potency. These findings suggest that the impairment of acetylcholine-induced relaxation in the diabetic state is not caused by the diminished production of an endethelium-derived relaxing factor or nitric oxide but rather by the increased endothellum-derived contracting factor or postaglandin [H.sub.2], which may be responsible for abnormalities of the vasculature in diabetes. Diabetes, Control of vascular tone has been shown to be modulated by various vasoactive substances produced by the endothelium such as EDRFs (1-3) and EDCFs (4) in response to various stimuli. [...]

Published
1993

21. Angiographic no-reflow phenomenon as a predictor of adverse long-term outcome in patients treated with percutaneous transluminal coronary angioplasty for first acute myocardial infarction

Author

Morishima, Itsuro, primary, Sone, Takahito, additional, Okumura, Kenji, additional, Tsuboi, Hideyuki, additional, Kondo, Junichiro, additional, Mukawa, Hiroaki, additional, Matsui, Hideo, additional, Toki, Yukio, additional, Ito, Takayuki, additional, and Hayakawa, Tetsuo, additional

Published
2000
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25. Simultaneous Intravascular Two-Dimensional Plus Doppler Ultrasound Is Useful for Evaluation of Postischemic Vasodilatation: Plasma NOx- Levels Determined by the Griess Method May Not Reflect the Extent of Postischemic NO-Induced Vasodilatation.

Author

HAYAKAWA, Makoto, primary, ITO, Takayuki, additional, OSANAI, Hiroyuki, additional, HARADA, Mitsunori, additional, NUMAGUCHI, Yasushi, additional, MOKUNO, Shinji, additional, MURASE, Kichiro, additional, and TOKI, Yukio, additional

Published
2000
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30. Prostacyclin Synthase Gene Transfer Accelerates Reendothelialization and Inhibits Neointimal Formation in Rat Carotid Arteries After Balloon Injury

Author

Numaguchi, Yasushi, primary, Naruse, Keiji, additional, Harada, Mitsunori, additional, Osanai, Hiroyuki, additional, Mokuno, Shinji, additional, Murase, Kichiro, additional, Matsui, Hideo, additional, Toki, Yukio, additional, Ito, Takayuki, additional, Okumura, Kenji, additional, and Hayakawa, Tetsuo, additional

Published
1999
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45. Identification of endothelium-derived contracting factor 1

Author

Muramatsu, Masahito, primary, Shimizu, Kiyokazu, additional, Asano, Hiroshi, additional, Iwama, Yoshio, additional, Toki, Yukio, additional, Miyazaki, Yutaka, additional, Okumura, Kenji, additional, Hashimoto, Hidekazu, additional, and Ito, Takayuki, additional

Published
1992
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47. Prostacyclin synthase gene transfer inhibits neointimal formation in rat balloon-injured arteries without bleeding complications.

Author

Harada, Mitsunori, Toki, Yukio, Numaguchi, Yasushi, Osanai, Hiroyuki, Ito, Takayuki, Okumura, Kenji, and Hayakawa, Tetsuo

Abstract

Objective: This study was designed to compare the effects of prostacyclin synthase (PCS) gene transfer with those of a systemic infusion of beraprost sodium (BPS), a prostacyclin analogue, on vascular smooth muscle cell (VSMC) proliferation and neointimal formation after arterial injury. Methods: PCS gene (3 or 30 μg) was transfected into rat balloon-injured carotid arteries by a non-viral lipotransfection method. BPS (100 or 300 μg/kg/day) was subcutaneously infused with osmotic pumps after the injury. LacZ gene (30 μg) was used as a control. VSMC proliferation was estimated by the bromodeoxyuridine (BrdU) index (BrdU-positive nuclei/total nuclei) at day 7. Neointimal formation was evaluated at day 14. Each treatment group had six rats. Results: PCS gene transfer prevented the increase in intimal/medial area ratio (3 μg: 46.6%, 30 μg: 61.1% reduction; P<0.05, P<0.01, respectively), as did BPS 300 μg/kg/day (49.8% reduction; P<0.05). BPS 100 μg/kg/day, however, had no effects on the ratio. PCS gene transfer and BPS 300 μg/kg/day significantly suppressed the BrdU index. BPS 300 μg/kg/day group had more frequent hematoma and longer bleeding time. There were no significant differences in blood pressure, heart rate, or urinary volume among all groups. Conclusion: Both PCS gene transfer and BPS 300 μg/kg/day reduced neointimal formation after arterial injury by inhibiting VSMC proliferation. PCS gene transfer may be a safer therapeutic modality against neointimal formation than a systemic infusion of BPS because the former method resulted in fewer bleeding complications. [ABSTRACT FROM PUBLISHER]

Published
1999
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48. Altered gene expression of prostacyclin synthase and prostacyclin receptor in the thoracic aorta of spontaneously hypertensive rats.

Author

Numaguchi, Yasushi, Harada, Mitsunori, Osanai, Hiroyuki, Hayashi, Kazunori, Toki, Yukio, Okumura, Kenji, Ito, Takayuki, and Hayakawa, Tetsuo

Abstract

Objective: The aim of this study was to evaluate the possible role of prostacyclin (PGI2) in the pathogenesis of hypertension in spontaneously hypertensive rats (SHR). Methods: Measurement of mRNA and protein levels of PGH synthase (PGHS)-1, PGI2 synthase and the PGI2 receptor, in the thoracic aorta was performed in SHR aged 5, 10, 20, and 40 weeks old and in age-matched normotensive Wistar–Kyoto (WKY) rats with a competitive polymerase chain reaction method and immunoblotting. Aortic production of 6-keto-PGF1α, the main metabolite of PGI2, was also measured. Results: Compared with age-matched WKY rats, PGHS-1 mRNA and protein levels in the thoracic aorta of SHR increased with age, reaching three- and twofold higher than WKY rats at 40 weeks old, respectively. PGI2 synthase mRNA and protein levels in SHR were significantly higher than in WKY rats at 20 and 40 weeks old. In contrast, PGI2 receptor mRNA levels in SHR were consistently lower than in WKY rats at all ages. Conclusions: These results provide evidence that hypertension elicits alterations in levels of arachidonic acid metabolites, including PGH2 and PGI2. They also suggest that the decreased expression of PGI2 receptor mRNA in prehypertensive SHR could be one of the causes of hypertension in SHR. [ABSTRACT FROM PUBLISHER]

Published
1999
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50. Changes in ventricular 1,2-diacylglycerol content in rats following monocrotaline treatment.

Author

Okumura, Kenji, Kondo, Junichiro, Shimizu, Kiyokazu, Yoshino, Mitsuhiko, Toki, Yukio, Hashimoto, Hidekazu, and Ito, Takayuki

Abstract

Objective: 1,2-Diacylglycerol may initiate cardiac hypertrophy, probably by activating protein kinase C. To test this hypothesis we determined the 1,2-diacylglycerol content of hypertrophied tissue. Methods: Rats were treated with monocrotaline and developed severe right ventricular hypertrophy followed by congestive heart failure. 1,2-Diacylglycerol content and fatty acid composition, DNA concentrations, and RNA concentrations in the right ventricle from monocrotaline treated rats were compared with values obtained from the left side or from control rats. Results: During the first week, the right ventricle showed no significant change in 1,2-diacylglycerol content and a small increase in RNA concentration. However, the 1,2-diacylglycerol content was significantly increased by 55% at two weeks after monocrotaline injection, when DNA and RNA synthesis was also enhanced to its highest level when compared with control rats (37% and 18%, respectively). At four weeks after monocrotaline injection, conversely, the 1,2-diacylglycerol content was decreased by 25% in the right ventricle from monocrotaline treated rats, most of which had pleural and peritoneal effusions indicating congestive heart failure, although RNA synthesis was sustained at a high level. The fatty acid composition of 1,2-diacylgylcerol did not differ significantly between the right and left ventricles or control rat ventricles. Conclusions: These results suggest that 1,2-diacylglycerol accumulation is associated with development of hypertrophy in monocrotaline treated rats. In contrast, at a stage of congestive heart failure 1,2-diacylglycerol production decreased, suggesting that intracellular transduction mechanisms may be attenuated. [ABSTRACT FROM PUBLISHER]

Published
1992

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