Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Protection against lipopolysaccharide-induced endothelial dysfunction in resistance and conduit vasculature of iNOS knockout mice.

FASEB journal : official publication of the Federation of American Societies for Experimental Biology - 1 Apr 2003

Chauhan S D, Seggara G, Vo P A, Macallister R J, Hobbs A J, Ahluwalia A

Abstract excerpt

Endothelial dysfunction is a characteristic of, and may be pathogenic in, inflammatory cardiovascular diseases, including sepsis. The mechanism underlying inflammation-induced endothelial dysfunction may be related to the expression and activity of inducible nitric oxide synthase (iNOS). This possibility was investigated in isolated resistance (mesenteric) and conduit (aorta) arteries taken from...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Arteries
Share to Nitric Oxide Donors

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Nitrites

Share to Norepinephrine

Share to Spermine

Share to Vasoconstriction

Share to Vasoconstrictor Agents

Share to Vasodilator Agents

Source

Identifiers

PMID: 12586741
DOI: 10.1096/fj.02-0668fje

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Protection against lipopolysaccharide-induced endothelial dysfunction in resistance and conduit vasculature of iNOS knockout mice.PMID 12586741Read ↗

Deletion of inducible nitric oxide synthase decreases mesenteric vascular responsiveness in portal hypertensive mice.Semantic proximity Read ↗

Perivascular adipose tissue phenotype and sepsis vascular dysfunction: Differential contribution of NO, ROS and beta 3-adrenergic receptor.Semantic proximity Read ↗

Lipopolysaccharide exposure modulates the contractile and migratory phenotypes of vascular smooth muscle cells.Semantic proximity Read ↗

Antihypertensive effects of inducible nitric oxide synthase inhibition in experimental pre‐eclampsiaSemantic proximity Read ↗

Cardioprotective function of inducible nitric oxide synthase and role of nitric oxide in myocardial ischemia and preconditioning: an overview of a decade of research.Semantic proximity Read ↗

An endothelium-derived hyperpolarizing factor-like factor moderates myogenic constriction of mesenteric resistance arteries in the absence of endothelial nitric oxide synthase-derived nitric oxide.Semantic proximity Read ↗

Redox signaling and splicing dependent change in myosin phosphatase underlie early versus late changes in NO vasodilator reserve in a mouse LPS model of sepsis.Semantic proximity Read ↗

Compensation of endothelium-dependent responses in coronary circulation of eNOS-deficient mice.Semantic proximity Read ↗

Essential roles of S-nitrosothiols in vascular homeostasis and endotoxic shock.Semantic proximity Read ↗

Disruption of Physiological Balance Between Nitric Oxide and Endothelium-Dependent Hyperpolarization Impairs Cardiovascular Homeostasis in Mice.Semantic proximity Read ↗

Gene knockout of the KCNJ8-encoded Kir6.1 K(ATP) channel imparts fatal susceptibility to endotoxemia.Semantic proximity Read ↗

Role of inducible nitric oxide synthase in endotoxin-induced acute lung injury.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.