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

Deletion of inducible nitric oxide synthase decreases mesenteric vascular responsiveness in portal hypertensive mice.

European journal of pharmacology - 24 Sept 2004

Bexis Sotiria, Vandeputte Catherine, McCormick P Aiden, Docherty James R

Abstract excerpt

The effects of pre-hepatic portal hypertension were examined on the responsiveness of aorta and mesenteric artery from wild-type, inducible nitric oxide synthase knockout (iNOS-KO) and endothelial nitric oxide synthase knockout (eNOS-KO) mice. Mice were sham-operated or made portal hypertensive by creating a calibrated portal vein stenosis. Acetylcholine produced marked relaxations in phenylephrine (10 microM)...

Read the complete abstract on PubMed

Topics

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

Share to Hypertension, Portal
Share to Microspheres

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to NG-Nitroarginine Methyl Ester

Share to Phenylephrine

Share to Potassium Chloride

Share to Vasoconstriction

Share to Vasoconstrictor Agents

Share to Vasodilator Agents

Source

Identifiers

PMID: 15381055
DOI: 10.1016/j.ejphar.2004.08.001

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

Deletion of inducible nitric oxide synthase decreases mesenteric vascular responsiveness in portal hypertensive mice.PMID 15381055Read ↗

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 ↗

Acetylcholine-induced relaxation in blood vessels from endothelial nitric oxide synthase knockout mice.Semantic proximity Read ↗

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

Role of endothelial nitric oxide synthase in the development of portal hypertension in the carbon tetrachloride-induced liver fibrosis model.Semantic proximity Read ↗

Hypertension in mice lacking the gene for endothelial nitric oxide synthase.Semantic proximity Read ↗

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

Altered reactivity of resistance vasculature contributes to hypertension in elastin insufficiency.Semantic proximity Read ↗

Investigation of vascular responses in endothelial nitric oxide synthase/cyclooxygenase-1 double-knockout mice: key role for endothelium-derived hyperpolarizing factor in the regulation of blood pressure in vivo.Semantic proximity Read ↗

Vascular function of the mesenteric artery isolated from thyroid hormone receptor-α knockout mice.Semantic proximity Read ↗

Elevated blood pressures in mice lacking endothelial nitric oxide synthase.Semantic proximity Read ↗

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

The alpha2-isoform of Na-K-ATPase mediates ouabain-induced hypertension in mice and increased vascular contractility in vitro.Semantic proximity Read ↗

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