Vasodilatation in the Canine Leg caused by Intra-arterial Infusion of Thrombin and Tissue Thromboplastin

Delin, A; Olsson, Per; Teger‐Nilsson, Ann‐Catrine

doi:10.1093/cvr/1.4.371

Cited by 21 publications

(16 citation statements)

References 22 publications

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“…Thrombin has earlier been shown to decrease the vascular resistance when injected into the femoral artery [2,12]. In the present series of ex periments, infusion of thrombin into the renal artery caused a decrease in renal blood flow, as well as a decrease in urine production.…”

Section: Discussionsupporting

confidence: 57%

“…As already discussed, the splitting off of fibrinopeptides is a relatively slow process at the low thrombin concentrations that we used. Infused into the femoral artery, homologous fibrinopeptides did not change the peripheral resistance in the hindlimb of the dog [2], Thrombin is reported to release several substances from platelets [6], in cluding A D P and serotonin. A vasodilator effect of thrombin, infused into the femoral artery, has been shown to be mediated by AD P/A TP released from blood cells [13J.…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies have, however, demonstrated that intravascular coagulation may act on the circulation via other path ways. Small amounts of thrombin infused into the femoral artery of the dog produce a pronounced decrease in regional vascular resistance [2,12], This decrease is mediated mainly by AD P/A TP, released from blood cells by thrombin [13], In view of this action by thrombin on the periph eral circulation, we have thought it of interest to investigate the effects of thrombinaemia on the kidney.…”

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confidence: 99%

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The Effect of Regional Thrombin Infusion on the Renal Vascular Resistance

1970

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Section: Discussionsupporting

confidence: 57%

Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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The Effect of Regional Thrombin Infusion on the Renal Vascular Resistance

1970

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“…Inactivation of thrombin by antithrombin III and/or hirudin has been reported by others (Joyner et al, 1973;Verhaeghe and Janssens, 1981). In addition, inactivation of thrombin with the proteolytic inhibitor diisopropyl fluorophosphate inhibited thrombin-induced vasodilation (Delin et al, 1967), whereas the binding of thrombin to endothelial cells was unaffected by diisopropyl fluorophosphate pretreatment (Awbrey et al, 1979).…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of adenosine triphosphate-, thrombin-, and trypsin-induced relaxation of rat thoracic aorta.

Rapoport¹,

Draznin²,

Murad³

1984

Circulation Research

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SUMMARY. The mechanisms by which adenosine triphosphate, thrombin, and trypsin cause relaxation of vascular smooth muscle were investigated. Relaxation of the rat thoracic aorta with adenosine triphosphate, thrombin, and/or trypsin was associated with increased levels of cyclic guanosine monophosphate in both time-and concentration-dependent manners. Thrombin and trypsin did not alter cyclic adenosine monophosphate levels, whereas adenosine triphosphate increased cyclic adenosine monophosphate levels after significant relaxation occurred. Removal of the endothelium abolished adenosine triphosphate-, thrombin-, and trypsin-induced relaxation and the associated increased levels of cyclic nucleotides. Relaxation due to these agents was also inhibited by exposure to nordihydroguaiaretic acid, a lipoxygenase inhibitor, and eicosatetraynoic acid, a lipoxygenase and cyclooxygenase inhibitor. Indomethacin, a cyclooxygenase inhibitor, potentiated relaxation to these agents, whereas the increased levels of cyclic nucleotides due to adenosine triphosphate were unaltered. Bromophenacyl bromide, a phospholipase A 2 inhibitor, decreased relaxation due to adenosine triphosphate, thrombin, and trypsin and the associated increased levels of cyclic nucleotides. Removal of extracellular calcium, which also presumably inhibits phospholipase A2, prevented the elevated levels of cyclic nucleotides and the inhibitory effects of adenosine triphosphate and trypsin on contraction. In contrast, sodium nitroprussideinduced relaxation and/or increased levels of cyclic guanosine monophosphate were unaltered by nordihydroguaiaretic acid, eicosatetraynoic acid, bromophenacyl bromide, and removal of extracellular calcium. After incubation of intact tissue with 32 P-orthophosphate, the patterns of protein phosphorylation caused by adenosine triphosphate, thrombin, and trypsin were indistinguishable from those of acetylcholine, sodium nitroprusside and 8-bromo cyclic guanosine monophosphate. All these agents dephosphorylated myosin light chain. Thus, the present study supports the hypothesis that relaxation induced by adenosine triphosphate, thrombin, and trypsin is mediated through the formation of an endothelial factor which elevates cyclic guanosine monophosphate levels and causes cyclic guanosine monophosphate-dependent protein phosphorylation and dephosphorylation of myosin light chain. (Circ Res 55: 468-479, 1984) ENDOTHELIUM-dependent vasodilation induced by acetylcholine, histamine and Ca ++ ionophore A23187 has recently been shown to be associated with the formation of cyclic guanosine monophosphate (cGMP) in both a time-and concentrationdependent manner in rat thoracic aorta . Furthermore, an inhibitor of phospholipase A 2 , quinacrine, and an inhibitor of lipoxygenase and cyclooxygenase, eicosatetraynoic acid (ETYA), inhibited acetylcholine-induced relaxation and the formation of cGMP . These results confirmed those of others (Furchgott and Zawadzki, 1980a;Furchgott et al., 1981;Furchgott, 1983) which suggested that relaxation cause...

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“…Infusion of thrombin into the bloodstream would, therefore, be expected to cause an increase in resistance to blood flow due to (partial) obstruction of blood vessels. This is true with high concen trations of the enzyme [Delin et al, 1967], but at lower concentrations an increase in blood flow through the hindleg or a drop in systemic blood pressure is observed, depend ing on the site of administration [Delin et al, 1967;-Joyner et al. 1973;Olsson et al, 1969a.…”

Section: Introductionmentioning

confidence: 99%

Effect of Thrombin on Isolated Canine Blood Vessels

Janssens¹,

Verhaeghe²

1982

J Vasc Res

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The aim of the present study was to assess whether or not thrombin affects vascular smooth muscle activity by a direct action on the blood vessel wall. In isolated saphenous veins and femoral and pulmonary arteries thrombin did not affect basal tension, but in pulmonary and portal mesenteric veins it caused contraction. In saphenous and femoral veins and in femoral and pulmonary arteries the enzyme depressed contractions evoked by α-adrenergic stimulation. In the saphenous vein thrombin also depressed contractions induced with acetylcholine or potassium ions. In this blood vessel the relaxation caused by thrombin was abolished by antithrombin III and the tripeptide D-phenylalanine-proline-arginine-CH2Cl, a specific inhibitor of the enzymatic center of thrombin. In pulmonary and portal mesenteric veins, thrombin potentiated the contractile response to norepinephrine. These contractile effects of thrombin were also abolished by D-phenylalanine-proline-arginine-CH2Cl. Thus, thrombin causes relaxation or contraction of blood vessels through a direct action on the blood vessel wall. These effects are due to its proteolytic activity.

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Vasodilatation in the Canine Leg caused by Intra-arterial Infusion of Thrombin and Tissue Thromboplastin

Cited by 21 publications

References 22 publications

The Effect of Regional Thrombin Infusion on the Renal Vascular Resistance

The Effect of Regional Thrombin Infusion on the Renal Vascular Resistance

Mechanisms of adenosine triphosphate-, thrombin-, and trypsin-induced relaxation of rat thoracic aorta.

Effect of Thrombin on Isolated Canine Blood Vessels

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