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

Smooth muscle specific deletion of Ndst1 leads to decreased vessel luminal area and no change in blood pressure in conscious mice.

Journal of cardiovascular translational research - 1 Jun 2012

Montaniel Kim Ramil C, Billaud Marie, Graham Cassandra, Kim Sun K, Carlson Marjorie, Zeng William, Zeng Orien, Pan Wei, Isakson Brant E, Hall Jennifer L, Adhikari Neeta

Abstract excerpt

Heparan sulfate proteoglycans are abundant matrix and membrane molecules. Smooth muscle specific deletion of one heparan sulfate biosynthetic enzyme, N-deacetylase-N-sulfotransferase1 leads to decreased vascular smooth muscle cell proliferation, and vascular wall thickness. We hypothesized that this may lead to changes in blood pressure in conscious mice. Blood pressure was measured via telemetry in...

Read the complete abstract on PubMed

Topics

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

Share to Aorta
Share to Blood Pressure Monitoring, Ambulatory

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Circadian Rhythm

Share to Heart Rate

Share to Integrases

Share to Muscle Proteins

Share to Muscle, Smooth, Vascular

Share to Sulfotransferases

Source

Open in PubMed Open full text

Identifiers

PMID: 22555965
DOI: 10.1007/s12265-012-9369-4
PMCID: PMC3381738

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Smooth muscle specific deletion of Ndst1 leads to decreased vessel luminal area and no change in blood pressure in conscious mice.PMID 22555965Read ↗

Enzymatically active N-deacetylase/N-sulfotransferase-2 is present in liver but does not contribute to heparan sulfate N-sulfation.Semantic proximity Read ↗

Collecting Duct Nitric Oxide Synthase 1ß Activation Maintains Sodium Homeostasis During High Sodium Intake Through Suppression of Aldosterone and Renal Angiotensin II Pathways.Semantic proximity Read ↗

Dimethylarginine dimethylaminohydrolase-1 is the critical enzyme for degrading the cardiovascular risk factor asymmetrical dimethylarginine.Semantic proximity Read ↗

Histone demethylase LSD1 deficiency during high-salt diet is associated with enhanced vascular contraction, altered NO-cGMP relaxation pathway, and hypertension.Semantic proximity Read ↗

Disturbed Ca2+ kinetics in N-deacetylase/N-sulfotransferase-1 defective myotubes.Semantic proximity Read ↗

Defective heparan sulfate biosynthesis and neonatal lethality in mice lacking N-deacetylase/N-sulfotransferase-1.Semantic proximity Read ↗

Null mutation of the nicotinamide adenine dinucleotide phosphate-oxidase subunit p67phox protects the Dahl-S rat from salt-induced reductions in medullary blood flow and glomerular filtration rate.Semantic proximity Read ↗

Structure of cerebral arterioles in mice deficient in expression of the gene for endothelial nitric oxide synthase.Semantic proximity Read ↗

Impact of Renal Denervation on Circadian Variations of Blood Pressure and Clock Gene Expression in Spontaneously Hypertensive RatsSemantic proximity Read ↗

A critical role for vascular smooth muscle in acute glucocorticoid-induced hypertension.Semantic proximity Read ↗

Heparan sulfate 2-O-sulfotransferase is required for triglyceride-rich lipoprotein clearance.Semantic proximity Read ↗

Failure to vasodilate in response to salt loading blunts renal blood flow and causes salt-sensitive hypertension.Semantic proximity Read ↗

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