Die Wirkung des Thrombins am Froschherzen

Markwardt, Fritz; Haustein, K.-O.; Nuernbergk, W

doi:10.1055/s-0038-1655612

Cited by 3 publications

(1 citation statement)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For the positive inotropic effect of thrombin on the isolated frog heart, identical concentration-response-relationships were obtained. 12,41 The serine protease trypsin mimics several of the actions of thrombin, for instance in platelets and vessels. In the isolated aorta from rats and rabbits and in canine coro nary arteries trypsin caused endothelium-dependent re laxation.…”

Section: Comparison With Other Cellular Activitiesmentioning

confidence: 99%

Vascular Effects of Thrombin

Glusa¹

1992

Semin Thromb Hemost

View full text Add to dashboard Cite

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...

show abstract

Section: Comparison With Other Cellular Activitiesmentioning

confidence: 99%

Vascular Effects of Thrombin

Glusa¹

1992

Semin Thromb Hemost

View full text Add to dashboard Cite

show abstract

Über die Freisetzung von Katecholaminen durch Thrombin

Markwardt

Nuernbergk

1965

Experientia

View full text Add to dashboard Cite

Effects of thrombin on single calcium channels in frog ventricular cells

et al. 1990

View full text Add to dashboard Cite

Single calcium channel (Ca channel) currents were measured using the patch-clamp technique in isolated ventricular myocytes of the frog (Rana esculenta). Sodium was used as the charge carrier. After formation of cell-attached patches, the proteolytic enzyme thrombin was added to the bath solution, where it increased the amplitude of the averaged currents more than twofold, by decreasing the number of empty sweeps and reducing the time constant of the slow exponential term of the shut-time histogram. Single channel conductance was not changed by thrombin. If the activation kinetics of the Ca channels are described by the commonly used C1-C2-O model, where C1 and C2 indicate closed states 1 and 2 respectively and O denotes the open state, thrombin increases the open-state probability in the non-empty sweeps by increasing the rate constant (k1) for the transition from C1 to C2. It is shown that thrombin acts via an H-7 blockable pathway.

show abstract

Die Wirkung des Thrombins am Froschherzen

Cited by 3 publications

References 0 publications

Vascular Effects of Thrombin

Vascular Effects of Thrombin

Über die Freisetzung von Katecholaminen durch Thrombin

Effects of thrombin on single calcium channels in frog ventricular cells

Contact Info

Product

Resources

About