Thrombin-induced endothelium-dependent relaxation and its inhibition by LDL in porcine coronary arteries.

Inoue, Yasuo; Tomita, Takako; Nakamura, Kazuki; Ezaki, Masanori; Nakayama, Koichi

doi:10.1248/cpb.36.4626

CHEMICAL & PHARMACEUTICAL BULLETIN

1988

DOI: 10.1248/cpb.36.4626

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Thrombin-induced endothelium-dependent relaxation and its inhibition by LDL in porcine coronary arteries.

Yasuo Inoue

Takako Tomita

Kazuki Nakamura

et al.

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Cited by 5 publications

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“…31 Thrombininduced endothelium-dependent relaxation has been demonstrated in isolated rat aorta, in porcine pulmonary and coronary arteries, in canine femoral, pulmonary, basilar, cerebral and saphenous arteries, and in human basilar and internal mammary arteries. 24,[28][29][30][32][33][34][35][36] How ever, in veins with intact endothelium the relaxation was less pronounced, in most cases an increase in tension was observed. 32,34,37,38 In isolated porcine coronary arteries thrombin caused reversible and transient relaxation of prostaglandin F 2α (PGF 2α )-precontracted vessels with in tact endothelium (Fig.…”

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Vascular Effects of Thrombin

Glusa¹

1992

Semin Thromb Hemost

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The proteolytic enzyme thrombin catalyzes the con version of fibrinogen to fibrin and activates clotting fac tors that are necessary for prothrombin transformation, fibrin stabilizing Factor XIII, and protein C activation. Thrombin is a potent activator of a variety of cell events and has been shown to evoke a number of physiologic responses in various tissues that are typical of those stim ulated by hormones. 1,2 It triggers several receptor-medi ated processes such as platelet aggregation, secretion, and formation of thromboxane A 2 3,4 and contraction of smooth muscle. 5,6 Furthermore, thrombin causes prolif eration of fibroblasts and osteoblastic cells, chemotaxis of monocytes, mitogenesis of neuroblastoma, and mesangial cells. 7-11 At very low concentrations, it stimu lates isolated frog heart muscle cells via activation of L-type calcium channels, presumably mediated by a sec ond messenger. 12 In the circulation thrombin is rapidly bound to high-affinity binding sites on endothelial cells. [13][14][15] It exerts various effects on these cells, such as release of plasminogen activator, platelet activating fac tor (PAF), endothelin, prostacyclin, and the so-called endothelium-derived relaxant factor (EDRF). 16-25 Pros tacyclin and EDRF cause vasodilation and inhibition of platelet aggregation. Therefore, thrombin may produce biphasic effects on vascular smooth muscle, endothelium-dependent vasodilation, or vasoconstriction. 26,27 The biphasic vascular effects depend on the anatomic origin and type of vessel and the species studied. 28-30 ENDOTHELIUM-DEPENDENT VASODILATIONSeveral endogenous substances such as acetylcho line and bradykinin, as well as the proteolytic enzymes thrombin and trypsin, are able to produce endotheliumdependent vasodilation indirectly mediated by EDRF re leased from the endothelium. The EDRF, which has been characterized as nitric oxide, activates the soluble guanylate cyclase in smooth muscle cells and increases the cyclic guanosine monophosphate (cGMP) level, thereby inducing relaxation of the smooth muscle. 31 Thrombininduced endothelium-dependent relaxation has been demonstrated in isolated rat aorta, in porcine pulmonary and coronary arteries, in canine femoral, pulmonary, basilar, cerebral and saphenous arteries, and in human basilar and internal mammary arteries. 24,[28][29][30][32][33][34][35][36] How ever, in veins with intact endothelium the relaxation was less pronounced, in most cases an increase in tension was observed. 32,34,37,38 In isolated porcine coronary arteries thrombin caused reversible and transient relaxation of prostaglandin F 2α (PGF 2α )-precontracted vessels with in tact endothelium (Fig. 1). The threshold concentration of thrombin to obtain significant relaxation was 0.01 U/ml (about 0.1 nmol/liter). The relaxant effect reached a max imum within 1 to 3 minutes and was gradually attenuated up to the initial tension. When the same thrombin con centration was added to the contracted vessel after the relaxant phase, no response was obtained on the second exp...

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confidence: 99%

Vascular Effects of Thrombin

Glusa¹

1992

Semin Thromb Hemost

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Endothelium-dependent relaxant effect of thrombocytin, a serine proteinase from Bothrops atrox snake venom, on isolated pig coronary arteries

Glusa

Brauns

Stocker³

1991

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Oral Warfarin and the Thrombin Inhibitor Dabigatran Increase Blood Pressure in Rats: Hidden Danger of Anticoagulants?

Ware

Vance

Muni

et al. 2014

American Journal of Hypertension

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Thrombin-induced endothelium-dependent relaxation and its inhibition by LDL in porcine coronary arteries.

Cited by 5 publications

References 0 publications

Vascular Effects of Thrombin

Vascular Effects of Thrombin

Endothelium-dependent relaxant effect of thrombocytin, a serine proteinase from Bothrops atrox snake venom, on isolated pig coronary arteries

Oral Warfarin and the Thrombin Inhibitor Dabigatran Increase Blood Pressure in Rats: Hidden Danger of Anticoagulants?

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