1999
DOI: 10.1161/01.hyp.33.6.1431
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Bradykinin Stimulates Tissue Plasminogen Activator Release in Human Vasculature

Abstract: Abstract-Bradykinin stimulates tissue plasminogen activator (tPA) release in isolated perfused animal tissues. The present study tests the hypothesis that bradykinin increases tPA release in humans through local effects on the vasculature. Graded doses of sodium nitroprusside (0.8 to 3.2 g/min), acetylcholine (ACh) (7.5 to 60 g/min), and bradykinin (100 to 400 ng/min) were administered intra-arterially in random order in 10 salt-depleted (10 mmol/d of Na) normotensive volunteers. None of the drugs altered mean… Show more

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Cited by 150 publications
(119 citation statements)
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“…Several products formed during thrombus formation, i.e. thrombin and FVa as well as bradykinin and plateletactivating factor are potent inducers of t-PA release [42,43,46,47]. The same holds true for substances formed during tissue ischemia, and possibly ischemia per se [48][49][50][51][52].…”
Section: Regulation Of Intravascular Fibrinolysis In Vivomentioning
confidence: 99%
“…Several products formed during thrombus formation, i.e. thrombin and FVa as well as bradykinin and plateletactivating factor are potent inducers of t-PA release [42,43,46,47]. The same holds true for substances formed during tissue ischemia, and possibly ischemia per se [48][49][50][51][52].…”
Section: Regulation Of Intravascular Fibrinolysis In Vivomentioning
confidence: 99%
“…2,4 ACE inhibition alters fibrinolysis by decreasing angiotensin II formation, a potent stimulus for PAI-1 expression, 5 and also by reducing the enzymatic degradation of bradykinin, a potent stimulus of tPA release. 19,20 ACEIs have been shown to reduce circulating PAI-1 antigen in patients with risk factors for coronary artery disease 9,13,21 or after myocardial infarction. 11,22 In addition, ACE inhibition prevents the increase in PAI-1 after thrombolysis.…”
Section: Pretorius Et Al Ace Inhibition Pai-1 and Cardiopulmonary Bmentioning
confidence: 99%
“…CPB stimulates the kallikrein-kinin system, increasing bradykinin concentrations 10-to 20-fold. 23,24 Because bradykinin stimulates endothelial tPA release, 19,20 decreased bradykinin clearance during ACE inhibition would be expected to increase tPA. Thus, the net effect of ACE inhibition in patients undergoing elective CABG requiring CPB was to increase fibrinolytic activity by decreasing PAI-1 antigen and increasing tPA antigen.…”
Section: Pretorius Et Al Ace Inhibition Pai-1 and Cardiopulmonary Bmentioning
confidence: 99%
“…Unlike ARBs that do not affect the metabolism of bradykinin, ACE-Is may exert a beneficial effect on fibrinolysis by blocking the degradation of bradykinin, which stimulates t-PA synthesis and release from endothelial cells through a bradykinin type-2 receptor-dependent pathway. 10,11 The dissimilar effects of imidapril and candesartan on PAI-1 could have been due in part to increased PAI-1 expression by the hexapeptide Ang II metabolite Ang IV and to stimulation of AT4 receptor, as reported in vitro in human endothelial cells. 52 These effects could have increased PAI-1 antigen concentration after short-term AT1 receptor blockade and after 2 week AT1 blockade, when AT4 receptors may be upregulated.…”
Section: Discussionmentioning
confidence: 99%
“…8 Aldosterone is another factor through which the rennin-angiotensin-aldosterone system may influence PAI-1 level, as demonstrated in vitro and in vivo. 1, 9 Because bradykinin increases the release of t-PA from endothelial cells, 10,11 angiotensin converting enzyme (ACE), which degrades bradykinin and catalyzes the conversion of Ang I to Ang II, might contribute to the reduction in t-PA production.…”
Section: Introductionmentioning
confidence: 99%