ArticleEndocrinology2009
Global disturbances in autonomic function yield cardiovascular instability and hypertension in the chromogranin a null mouse.
Article in Endocrinology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
41 citing papers in PubMed, 66 citations in OpenAlex.
- Catestatin restores cardiac metabolic flexibility and enhances mitochondrial function.Communications biology · 2026Article
- A complex role of chromogranin A and its peptides in inflammation, autoimmunity, and infections.Frontiers in immunology · 2025Review
- Plasma catestatin levels are related to metabolic parameters in patients with essential hypertension and type 2 diabetes mellitus.Heart and vessels · 2024Article
- Determination of Catecholamines in a Small Volume (25 μL) of Plasma from Conscious Mouse Tail Vein.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Serum chromogranin A levels are associated with the SYNTAX score in coronary artery disease.Revista da Associacao Medica Brasileira (1992) · 2023Article
- The association of catestatin and endocan with the effects of cardiac shock wave therapy: Biomarker sub-study of the randomized, sham procedure-controlled trial.Frontiers in cardiovascular medicine · 2023Article
- Catestatin induces glycogenesis by stimulating the phosphoinositide 3-kinase-AKT pathway.Acta physiologica (Oxford, England) · 2022Article
- Putative regulation of macrophage-mediated inflammation by catestatin.Trends in immunology · 2022Review
- Role of Catestatin in the Cardiovascular System and Metabolic Disorders.Frontiers in cardiovascular medicine · 2022Review
- Review
- Differential Antihypertensive Effects of Oral Doses of Acetylcholine between Spontaneously Hypertensive Rats and Normotensive Rats.Foods (Basel, Switzerland) · 2021Article
- Role and function of granin proteins in diabetes mellitus.World journal of diabetes · 2021Review
- Catestatin reverses the hypertrophic effects of norepinephrine in H9c2 cardiac myoblasts by modulating the adrenergic signaling.Molecular and cellular biochemistry · 2020Article
- Chromogranin A and its fragments in cardiovascular, immunometabolic, and cancer regulation.Annals of the New York Academy of Sciences · 2019Review
- Catestatin in Acutely Decompensated Heart Failure Patients: Insights from the CATSTAT-HF Study.Journal of clinical medicine · 2019Article
- Cardiomyokines from the heart.Cellular and molecular life sciences : CMLS · 2018Review
- Catestatin Induces Glucose Uptake and GLUT4 Trafficking in Adult Rat Cardiomyocytes.BioMed research international · 2018Article
- Catestatin as a Target for Treatment of Inflammatory Diseases.Frontiers in immunology · 2018Review
- Glycosylated Chromogranin A: Potential Role in the Pathogenesis of Heart Failure.Current heart failure reports · 2017Review
- Chromogranin A regulates vesicle storage and mitochondrial dynamics to influence insulin secretion.Cell and tissue research · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
We reported previously that chromogranin A (Chga) knockout (KO) mice are hypertensive and hyperadrenergic. Here we sought to determine the basis of such alterations by probing physiological, biochemical, and pharmacological responses to perturbations of the autonomic nervous system. In the conscious state, KO mice had substantially elevated basal high blood pressure (BP) and heart rate (HR); immobilization stress caused increments in systolic BP and HR in both wild-type (WT) and KO mice, with higher maxima but blunted increments in the KO state. Catestatin (CST; CHGA(352-372)) selectively diminished stress-induced increments in BP and HR in KO mice, implicating CST as an antihypertensive peptide, even in stressful conditions. Heightened plasma catecholamines in KO mice returned to WT level after CST. Stress caused further increments in catecholamines in WT mice but no change in KO mice. KO mice displayed diminished baroreflex sensitivity in response to either phenylephrine or sodium nitroprusside, accounting for exaggerated pressor and depressor responses to these compounds; baroreceptor function was normalized by CST. To probe the relative roles of endogenous/basal sympathetic vs. parasympathetic tone in control of BP and HR, we used the muscarinic-cholinergic antagonist atropine or the beta-adrenergic antagonist propranolol; HR and BP responses to each antagonist were exaggerated in KO animals. We conclude that ablation of Chga expression results in global disturbances in autonomic function, both sympathetic and parasympathetic, that can be abrogated (or rescued), at least in part, by replacement of CST. The results point to mechanisms whereby CHGA and its CST fragment act to control cardiovascular homeostasis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.