Plasmin induces endothelium-dependent nitric oxide-mediated relaxation in the porcine coronary artery

Tetsuhiro Fujiyoshi, Katsuya Hirano, Mayumi Hirano, Junji Nishimura, Shosuke Takahashi, Hideo Kanaide

研究成果: ジャーナルへの寄稿記事

4 引用 (Scopus)

抄録

OBJECTIVE - Plasmin is a key enzyme in fibrinolysis. We attempted to determine the possible role of plasmin in the regulation of vascular tone, while also investigating the mechanism of plasmin-induced vasorelaxation. METHODS AND RESULTS - In porcine coronary artery, plasmin induced an endothelium-dependent relaxation. This relaxing effect was mostly abolished by a proteinase inhibitor, a plasmin inhibitor, or a nitric oxide (NO) synthase inhibitor. The preceding stimulation with plasmin significantly inhibited the subsequent relaxation induced by thrombin but not that induced by proteinase-activated receptor-1-activating peptide. The relaxation induced by trypsin and substance P remained unaffected by the preceding plasmin stimulation. The pretreatment with plasmin, thrombin, or trypsin significantly attenuated the plasmin-induced relaxation. In porcine coronary artery endothelial cells (PCAECs) and human umbilical vein endothelial cells (HUVECs), plasmin induced a transient elevation in the cytosolic Ca concentrations ([Ca]i). The preceding stimulation with plasmin inhibited the subsequent [Ca]i elevation induced by thrombin but not that induced by trypsin. In PCAECs, plasmin concentration-dependently induced NO production. CONCLUSIONS - The present study demonstrated, for the first time, that plasmin induced an endothelium-dependent NO-mediated relaxation in the porcine coronary artery, while also showing plasmin to specifically inactivate the thrombin receptor.

元の言語英語
ページ(範囲)949-954
ページ数6
ジャーナルArteriosclerosis, thrombosis, and vascular biology
27
発行部数4
DOI
出版物ステータス出版済み - 4 1 2007

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Fibrinolysin
Endothelium
Coronary Vessels
Nitric Oxide
Swine
Thrombin
Trypsin
Endothelial Cells
PAR-1 Receptor
Thrombin Receptors
Antifibrinolytic Agents
Human Umbilical Vein Endothelial Cells
Fibrinolysis
Substance P
Vasodilation
Nitric Oxide Synthase
Blood Vessels
Peptide Hydrolases

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

これを引用

Plasmin induces endothelium-dependent nitric oxide-mediated relaxation in the porcine coronary artery. / Fujiyoshi, Tetsuhiro; Hirano, Katsuya; Hirano, Mayumi; Nishimura, Junji; Takahashi, Shosuke; Kanaide, Hideo.

:: Arteriosclerosis, thrombosis, and vascular biology, 巻 27, 番号 4, 01.04.2007, p. 949-954.

研究成果: ジャーナルへの寄稿記事

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AU - Fujiyoshi, Tetsuhiro

AU - Hirano, Katsuya

AU - Hirano, Mayumi

AU - Nishimura, Junji

AU - Takahashi, Shosuke

AU - Kanaide, Hideo

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N2 - OBJECTIVE - Plasmin is a key enzyme in fibrinolysis. We attempted to determine the possible role of plasmin in the regulation of vascular tone, while also investigating the mechanism of plasmin-induced vasorelaxation. METHODS AND RESULTS - In porcine coronary artery, plasmin induced an endothelium-dependent relaxation. This relaxing effect was mostly abolished by a proteinase inhibitor, a plasmin inhibitor, or a nitric oxide (NO) synthase inhibitor. The preceding stimulation with plasmin significantly inhibited the subsequent relaxation induced by thrombin but not that induced by proteinase-activated receptor-1-activating peptide. The relaxation induced by trypsin and substance P remained unaffected by the preceding plasmin stimulation. The pretreatment with plasmin, thrombin, or trypsin significantly attenuated the plasmin-induced relaxation. In porcine coronary artery endothelial cells (PCAECs) and human umbilical vein endothelial cells (HUVECs), plasmin induced a transient elevation in the cytosolic Ca concentrations ([Ca]i). The preceding stimulation with plasmin inhibited the subsequent [Ca]i elevation induced by thrombin but not that induced by trypsin. In PCAECs, plasmin concentration-dependently induced NO production. CONCLUSIONS - The present study demonstrated, for the first time, that plasmin induced an endothelium-dependent NO-mediated relaxation in the porcine coronary artery, while also showing plasmin to specifically inactivate the thrombin receptor.

AB - OBJECTIVE - Plasmin is a key enzyme in fibrinolysis. We attempted to determine the possible role of plasmin in the regulation of vascular tone, while also investigating the mechanism of plasmin-induced vasorelaxation. METHODS AND RESULTS - In porcine coronary artery, plasmin induced an endothelium-dependent relaxation. This relaxing effect was mostly abolished by a proteinase inhibitor, a plasmin inhibitor, or a nitric oxide (NO) synthase inhibitor. The preceding stimulation with plasmin significantly inhibited the subsequent relaxation induced by thrombin but not that induced by proteinase-activated receptor-1-activating peptide. The relaxation induced by trypsin and substance P remained unaffected by the preceding plasmin stimulation. The pretreatment with plasmin, thrombin, or trypsin significantly attenuated the plasmin-induced relaxation. In porcine coronary artery endothelial cells (PCAECs) and human umbilical vein endothelial cells (HUVECs), plasmin induced a transient elevation in the cytosolic Ca concentrations ([Ca]i). The preceding stimulation with plasmin inhibited the subsequent [Ca]i elevation induced by thrombin but not that induced by trypsin. In PCAECs, plasmin concentration-dependently induced NO production. CONCLUSIONS - The present study demonstrated, for the first time, that plasmin induced an endothelium-dependent NO-mediated relaxation in the porcine coronary artery, while also showing plasmin to specifically inactivate the thrombin receptor.

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