NDLI: Temporal variation in endotoxin-induced vascular hyporeactivity in a rat mesenteric artery organ culture model

Content Provider	PubMed Central
Author	O'brien, A. J. Wilson, A. J. Sibbald, R. Singer, M. Clapp, L. H.
Copyright Year	2001
Abstract	Endotoxin-induced vascular hyporeactivity to phenylephrine (PE) is well described in rodent aorta, but has not been investigated in smaller vessels in vitro. Segments of rat superior mesenteric artery were incubated in culture medium with or without foetal bovine serum (10%) for 6, 20 or 46 h in the presence or absence of bacterial lipopolysaccharide (LPS; 1 – 100 μg ml−1). Contractions to PE were measured with or without nitric oxide synthase (NOS) inhibitors: L-NAME (300 μM), aminoguanidine (AMG; 400 μM) 1400W (10 μM) and GW273629 (10 μM); the guanylyl cyclase inhibitor, ODQ (3 μM); the COX-2 inhibitor, NS-398 (10 μM). Contractile responses to the thromboxane A2 mimetic, U46619 were also assessed. In the presence of serum, LPS induced hyporeactivity at all time points. In its absence, hyporeactivity only occurred at 6 and 20 h. L-NAME and AMG fully reversed hyporeactivity at 6 h, whereas they were only partially effective at 20 h and not at all at 46 h. In contrast partial reversal of peak contraction was observed with 1400W (62% at 46 h), GW273629 (57% at 46 h) and ODQ (75% at 46 h). COX-2 inhibition produced no reversal. In contrast to PE, contractions to U46619 were substantially less affected by LPS. We describe a well-characterized reproducible model of LPS-induced hyporeactivity, which is largely mediated by the NO-cyclic GMP-dependent pathway. Importantly, long-term (2-day) production of NO via iNOS is demonstrated. Moreover, conventional doses of L-NAME and AMG became increasingly ineffective over time. Thus, the choice of inhibitor merits careful consideration in long-term models.
Related Links	http://dx.doi.org/10.1038/sj.bjp.0704079
Ending Page	360
Page Count	10
Starting Page	351
File Format	PDF
ISSN	00071188
Journal	British Journal of Pharmacology
Issue Number	3
Volume Number	133
Language	English
Publisher Date	2001-06-01
Access Restriction	Open
Subject Keyword	Pharmacology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Pharmacology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Temporal variation in endotoxin-induced vascular hyporeactivity in a rat mesenteric artery organ culture model.

Inhibition of endotoxin-induced vascular hyporeactivity by 4-amino-tetrahydrobiopterin

Dependence of endotoxin-induced vascular hyporeactivity on extracellular L-arginine.

Mechanisms Underlying a Decrease in KCl-Induced Contraction after Long-TermSerum-Free Organ Culture of Rat Isolated Mesenteric Artery

Depletion of intracellular Ca2+ stores enhances flow-induced vascular dilatation in rat small mesenteric artery

Role of adventitial nitric oxide in vascular hyporeactivity induced by lipopolysaccharide in rat aorta

NO and KATP channels underlie endotoxin-induced smooth muscle hyperpolarization in rat mesenteric resistance arteries

Nitric oxide-dependent and -independent vascular hyporeactivity in mesenteric arteries of portal hypertensive rats

Involvement of ATP-sensitive potassium channels in a model of a delayed vascular hyporeactivity induced by lipopolysaccharide in rats

Temporal variation in endotoxin-induced vascular hyporeactivity in a rat mesenteric artery organ culture model

Similar Documents

Temporal variation in endotoxin-induced vascular hyporeactivity in a rat mesenteric artery organ culture model.

Inhibition of endotoxin-induced vascular hyporeactivity by 4-amino-tetrahydrobiopterin

Dependence of endotoxin-induced vascular hyporeactivity on extracellular L-arginine.

Mechanisms Underlying a Decrease in KCl-Induced Contraction after Long-TermSerum-Free Organ Culture of Rat Isolated Mesenteric Artery

Depletion of intracellular Ca2+ stores enhances flow-induced vascular dilatation in rat small mesenteric artery

Role of adventitial nitric oxide in vascular hyporeactivity induced by lipopolysaccharide in rat aorta

NO and KATP channels underlie endotoxin-induced smooth muscle hyperpolarization in rat mesenteric resistance arteries

Nitric oxide-dependent and -independent vascular hyporeactivity in mesenteric arteries of portal hypertensive rats

Involvement of ATP-sensitive potassium channels in a model of a delayed vascular hyporeactivity induced by lipopolysaccharide in rats

Temporal variation in endotoxin-induced vascular hyporeactivity in a rat mesenteric artery organ culture model