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

Regulation of atrial catecholamine enzymes and adrenoceptor gene expression after chronic stress

1 Dec 2011

Abstract excerpt

Chronic stress is a risk factor for the development of numerous psychopathological conditions in humans including depression. Changes in gene expression of tyrosine-hydroxylase (TH), dopamine-β-hydroxylase (DBH) phenylethanolamine N-methyltransferase (PNMT), β1-, β2- and β3-adrenoceptors in right and left rat atria upon chronic unpredictable mild stress (CMS) were investigated. CMS decreased TH and DBH gene...

Read the complete abstract on PubMed

Topics

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

Share to Hormonal Regulation and Hypertension
Share to Renin-Angiotensin System Studies
Share to Stress Responses and Cortisol

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 22173024
DOI: 10.1556/aphysiol.98.2011.4.6

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Regulation of atrial catecholamine enzymes and adrenoceptor gene expression after chronic stressPMID 22173024Read ↗

[Expression of Catechol-O-Methyltransferase (Comt), Mineralocorticoid Receptor (Mlr), and Epithelial Sodium Channel (ENaC) Genes in Kidneys of Hypertensive ISIAH Rats at Rest and during Response to Stress].Semantic proximity Read ↗

Drug-induced and genetic alterations in stress-responsive systems: Implications for specific addictive diseases.Semantic proximity Read ↗

Cardiac MAO-A inhibition protects against catecholamine-induced ventricular arrhythmias via enhanced diastolic calcium controlSemantic proximity Read ↗

α2δ-1-Dependent NMDA Receptor Activity in the Hypothalamus Is an Effector of Genetic-Environment Interactions That Drive Persistent Hypertension.Semantic proximity Read ↗

Pathogenesis of depression- and anxiety-like behavior in an animal model of hypertrophic cardiomyopathy.Semantic proximity Read ↗

Hypoxia and adrenergic function: molecular mechanisms related to Egr-1 and Sp1 activation.Semantic proximity Read ↗

Pharmacological modulations of adrenergic phenotype in medullary C2 and C3 cell groups of adult rat.Semantic proximity Read ↗

Clinical implications of genetic and acquired defects in catecholamine synthesis and metabolism.Semantic proximity Read ↗

Catecholamine biosynthetic enzyme expression in neurological and psychiatric disorders.Semantic proximity Read ↗

Increased stress response and β–phenylethylamine in MAOB–deficient miceSemantic proximity Read ↗

Epinephrine is required for normal cardiovascular responses to stress in the phenylethanolamine N-methyltransferase knockout mouse.Semantic proximity Read ↗

Expression of nitric oxide synthase isoforms in hypothalamo-pituitary-adrenal axis during the development of spontaneous hypertension in rats.Semantic proximity Read ↗

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