The recognition site for hepatic clearance of plasma kallikrein is on its heavy chain and is latent on prokallikrein

Borges, Durval Rosa; Kouyoumdjian, Maria

doi:10.1016/s0168-8278(05)80103-5

Cited by 22 publications

(21 citation statements)

References 19 publications

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“…Our results showed that tPA clearance from plasma decreases in turpentine-treated rats and that the AP response does not modify the in vivo tissue distribution of 125 I-tPA, with the liver being responsible for most of the 125 I-tPA cleared from the circulation even after an inflamma- tory stimulus. We assured that labeling of tPA with 125 I does not impair its clearance by the liver, a phenomenon described for plasma kallikrein (18).…”

Section: Discussionmentioning

confidence: 97%

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The hepatic clearance of recombinant tissue-type plasminogen activator decreases after an inflammatory stimulus

Nagaoka

Kouyoumdjian

Borges

2000

Braz J Med Biol Res

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We have shown that tissue-type plasminogen activator (tPA) and plasma kallikrein share a common pathway for liver clearance and that the hepatic clearance rate of plasma kallikrein increases during the acute-phase (AP) response. We now report the clearance of tPA from the circulation and by the isolated, exsanguinated and in situ perfused rat liver during the AP response (48-h ex-turpentine treatment). For the sake of comparison, the hepatic clearance of a tissue kallikrein and thrombin was also studied. We verified that, in vivo, the clearance of 125 I-tPA from the circulation of turpentine-treated rats (2.2 ± 0.2 ml/ min, N = 7) decreases significantly (P = 0.016) when compared to normal rats (3.2 ± 0.3 ml/min, N = 6). The AP response does not modify the tissue distribution of administered 125 I-tPA and the liver accounts for most of the 125 I-tPA (>80%) cleared from the circulation. The clearance rate of tPA by the isolated and perfused liver of turpentine-treated rats (15.5 ± 1.3 µg/min, N = 4) was slower (P = 0.003) than the clearance rate by the liver of normal rats (22.5 ± 0.7 µg/ min, N = 10). After the inflammatory stimulus and additional Kupffer cell ablation (GdCl 3 treatment), tPA was cleared by the perfused liver at 16.2 ± 2.4 µg/min (N = 5), suggesting that Kupffer cells have a minor influence on the hepatic tPA clearance during the AP response. In contrast, hepatic clearance rates of thrombin and pancreatic kallikrein were not altered during the AP response. These results contribute to explaining why the thrombolytic efficacy of tPA does not correlate with the dose administered.

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Section: Discussionmentioning

confidence: 97%

“…tPA labeling tPA (100 µg) in 0.05 M sodium phosphate, pH 7.4, was iodinated with 125 I (1 mCi) using the chloramine T method (18). Unincorporated iodine was removed by gel filtration on a PD-10 column and eluted with 50 mM sodium phosphate, pH 7.4.…”

Section: Inflammatory Stimulusmentioning

confidence: 99%

The hepatic clearance of recombinant tissue-type plasminogen activator decreases after an inflammatory stimulus

Nagaoka

Kouyoumdjian

Borges

2000

Braz J Med Biol Res

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“…15 Briefly, the rat was anesthetized with urethane, 1.3 g/ kg, intraperitoneally. (Sigma Chemical Co, St Louis, MO, USA).…”

Section: Monovascular Rat Liver Perfusionmentioning

confidence: 99%

Hepatic conversion of angiotensin I and the portal hypertensive response to angiotensin II in normal and regenerating liver

Carvalho¹,

Nascimento

Teixeira

et al. 2007

J of Gastro and Hepatol

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“…Monovascular rat liver perfusion was performed as previously described (11). Briefly, the rat was perfused with 50 mL Krebs-Henseleit-bicarbonate buffer containing 1.5 g/dL hemoglobin, and 1 g/dL bovine albumin at a 16-mL/min perfusion rate.…”

Section: Liver Perfusion Experimentsmentioning

confidence: 99%

The combination of atorvastatin and ethanol is not more hepatotoxic to rats than the administration of each drug alone

Ito

Molina

Andriolo

et al. 2007

Braz J Med Biol Res

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Animal studies and premarketing clinical trials have revealed hepatotoxicity of statins, primarily minor elevations in serum alanine aminotransferase levels. The combined chronic use of medicines and eventual ethanol abuse are common and may present a synergistic action regarding liver injury. Our objective was to study the effect of the chronic use of atorvastatin associated with acute ethanol administration on the liver in a rat model. One group of rats was treated daily for 5 days a week for 2 months with 0.8 mg/kg atorvastatin by gavage. At the end of the treatment the livers were perfused with 72 mM ethanol for 60 min. Control groups (at least 4 animals in each group) consisted of a group of 2-month-old male Wistar EPM-1 rats exposed to 10% ethanol (v/v) ad libitum replacing water for 2 months, followed by perfusion of the liver with 61 nM atorvastatin for 60 min, and a group of animals without chronic ethanol treatment whose livers were perfused with atorvastatin and/or ethanol. The combination of atorvastatin with ethanol did not increase the release of injury marker enzymes (alanine aminotransferase, aspartate aminotransferase, and lactic dehydrogenase) from the liver and no change in liver function markers (bromosulfophthalein clearance, and oxygen consumption) was observed. Our results suggest that the combination of atorvastatin with ethanol is not more hepatotoxic than the separate use of each substance.

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The recognition site for hepatic clearance of plasma kallikrein is on its heavy chain and is latent on prokallikrein

Cited by 22 publications

References 19 publications

The hepatic clearance of recombinant tissue-type plasminogen activator decreases after an inflammatory stimulus

The hepatic clearance of recombinant tissue-type plasminogen activator decreases after an inflammatory stimulus

Hepatic conversion of angiotensin I and the portal hypertensive response to angiotensin II in normal and regenerating liver

The combination of atorvastatin and ethanol is not more hepatotoxic to rats than the administration of each drug alone

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