icatibant and Hypertension--Portal

icatibant has been researched along with Hypertension--Portal* in 1 studies

Other Studies

1 other study(ies) available for icatibant and Hypertension--Portal

Article	Year
Fate of bradykinin on the rat liver when administered by the venous or arterial route. Journal of gastroenterology and hepatology, 2005, Volume: 20, Issue:3 Bradykinin (BK) infused into the portal vein elicits a hypertensive response via the B2 receptor (B2R) and is efficiently hydrolyzed by the liver. Our purpose was to characterize the mechanism of interaction between BK and the liver.. BK, HOE-140 (a B2R antagonist), des-R(9)-BK (a B1R agonist) and enzyme inhibitors were used in monovascular or bivascular perfusions and in isolated liver cell assays.. Des-R(9)-BK did not elicit a portal hypertensive response (PHR); BK infused into the hepatic artery elicited a calcium-dependent PHR and a calcium-independent arterial hypertensive response (HAHR), with the latter being almost abolished by naproxen. BK has a predominant distribution in the extracellular space and an average hepatic extraction of 8% in the steady state. Hydrolysis products of infused BK (R(1)-F(5) and R(1)-P(7)) did not elicit PHR. Angiotensin converting enzyme (ACE) is concentrated in the perivenous region and B2R in the periportal region. Microphysiometry showed that BK (and not a B1 agonist) interacts with stellate cells and the endothelial sinusoidal/Kupffer cell fraction. This effect was inhibited by the B2R antagonist.. Events can be summarized as: the hypertensive action of BK on sinusoidal cells of the periportal region is followed by its hydrolysis by ACE which is primarily present in the perivenous region; there is no functional B1R in the normal liver; BK induces HAHR via eicosanoid release and PHR by a distinct pathway on the B2R. Our data suggest that BK may participate in the modulation of sinusoidal microvasculature tonus both in the portal and the arterial routes. Topics: Adrenergic beta-Antagonists; Animals; Bradykinin; Bradykinin B2 Receptor Antagonists; Chromatography, High Pressure Liquid; Disease Models, Animal; Dose-Response Relationship, Drug; Extracellular Space; Fluorescent Antibody Technique; Hepatic Artery; Hydrolysis; Hypertension, Portal; Infusions, Intra-Arterial; Infusions, Intravenous; Kupffer Cells; Liver; Liver Circulation; Male; Mass Spectrometry; Peptidyl-Dipeptidase A; Portal Pressure; Portal Vein; Rats; Rats, Wistar; Receptor, Bradykinin B2	2005

Article

Year

Fate of bradykinin on the rat liver when administered by the venous or arterial route.

Journal of gastroenterology and hepatology, 2005, Volume: 20, Issue:3

Bradykinin (BK) infused into the portal vein elicits a hypertensive response via the B2 receptor (B2R) and is efficiently hydrolyzed by the liver. Our purpose was to characterize the mechanism of interaction between BK and the liver.. BK, HOE-140 (a B2R antagonist), des-R(9)-BK (a B1R agonist) and enzyme inhibitors were used in monovascular or bivascular perfusions and in isolated liver cell assays.. Des-R(9)-BK did not elicit a portal hypertensive response (PHR); BK infused into the hepatic artery elicited a calcium-dependent PHR and a calcium-independent arterial hypertensive response (HAHR), with the latter being almost abolished by naproxen. BK has a predominant distribution in the extracellular space and an average hepatic extraction of 8% in the steady state. Hydrolysis products of infused BK (R(1)-F(5) and R(1)-P(7)) did not elicit PHR. Angiotensin converting enzyme (ACE) is concentrated in the perivenous region and B2R in the periportal region. Microphysiometry showed that BK (and not a B1 agonist) interacts with stellate cells and the endothelial sinusoidal/Kupffer cell fraction. This effect was inhibited by the B2R antagonist.. Events can be summarized as: the hypertensive action of BK on sinusoidal cells of the periportal region is followed by its hydrolysis by ACE which is primarily present in the perivenous region; there is no functional B1R in the normal liver; BK induces HAHR via eicosanoid release and PHR by a distinct pathway on the B2R. Our data suggest that BK may participate in the modulation of sinusoidal microvasculature tonus both in the portal and the arterial routes.

Topics: Adrenergic beta-Antagonists; Animals; Bradykinin; Bradykinin B2 Receptor Antagonists; Chromatography, High Pressure Liquid; Disease Models, Animal; Dose-Response Relationship, Drug; Extracellular Space; Fluorescent Antibody Technique; Hepatic Artery; Hydrolysis; Hypertension, Portal; Infusions, Intra-Arterial; Infusions, Intravenous; Kupffer Cells; Liver; Liver Circulation; Male; Mass Spectrometry; Peptidyl-Dipeptidase A; Portal Pressure; Portal Vein; Rats; Rats, Wistar; Receptor, Bradykinin B2

2005