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

Endothelial nitric oxide gene knockout mice: cardiac phenotypes and the effect of angiotensin-converting enzyme inhibitor on myocardial ischemia/reperfusion injury.

Hypertension (Dallas, Tex. : 1979) - 1 Jul 1999

Yang X P, Liu Y H, Shesely E G, Bulagannawar M, Liu F, Carretero O A

Abstract excerpt

We tested the hypothesis that nitric oxide (NO) released by endothelial NO synthase (eNOS) is not only important in blood pressure regulation but also involved in cardiac function and remodeling and in the cardioprotective effect of angiotensin-converting enzyme inhibitors (ACEi). With the use of a 2D Doppler echocardiography system equipped with a 15-MHz linear transducer, we evaluated left ventricular (LV)...

Read the complete abstract on PubMed

Topics

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

Share to Angiotensin-Converting Enzyme Inhibitors
Share to Heart Rate

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Myocardial Ischemia

Share to Myocardial Reperfusion Injury

Share to Nitric Oxide Synthase

Share to Nitric Oxide Synthase Type II

Share to Ultrasonography, Doppler

Share to Ventricular Function, Left

Source

Identifiers

PMID: 10406819
DOI: 10.1161/01.hyp.34.1.24

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

Endothelial nitric oxide gene knockout mice: cardiac phenotypes and the effect of angiotensin-converting enzyme inhibitor on myocardial ischemia/reperfusion injury.PMID 10406819Read ↗

Endothelial nitric oxide synthase is not necessary for the early phase of ischemic preconditioning in the mouse.Semantic proximity Read ↗

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

Endothelial nitric oxide synthase limits left ventricular remodeling after myocardial infarction in mice.Semantic proximity Read ↗

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

Generation of a conditional allele for the mouse endothelial nitric oxide synthase gene.Semantic proximity Read ↗

Accelerated atherosclerosis, aortic aneurysm formation, and ischemic heart disease in apolipoprotein E/endothelial nitric oxide synthase double-knockout mice.Semantic proximity Read ↗

Endothelial nitric oxide synthase gene: prospects for treatment of heart disease.Semantic proximity Read ↗

Endothelial dysfunction and elevated blood pressure in MAS gene-deleted mice.Semantic proximity Read ↗

Myocardial contractile function and heart rate in mice with myocyte-specific overexpression of endothelial nitric oxide synthase.Semantic proximity Read ↗

Blood pressures and cardiovascular homeostasis in mice having reduced or absent angiotensin-converting enzyme gene function.Semantic proximity Read ↗

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

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

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