natriuretic-peptide--c-type and Atrial-Fibrillation

natriuretic-peptide--c-type has been researched along with Atrial-Fibrillation* in 3 studies

Other Studies

3 other study(ies) available for natriuretic-peptide--c-type and Atrial-Fibrillation

ArticleYear
Natriuretic Peptide Receptor B Protects Against Atrial Fibrillation by Controlling Atrial cAMP Via Phosphodiesterase 2.
    Circulation. Arrhythmia and electrophysiology, 2023, Volume: 16, Issue:11

    β-AR (β-adrenergic receptor) stimulation regulates atrial electrophysiology and Ca. Studies were performed using atrial samples from human patients with AF or sinus rhythm and in wild-type and NPR-B-deficient (NPR-B. Atrial NPR-B protein levels were reduced in patients with AF, and NPR-B. NPR-B protects against AF by preventing enhanced atrial responses to β-adrenergic receptor agonists.

    Topics: Animals; Atrial Fibrillation; Heart Atria; Humans; Isoproterenol; Mice; Myocytes, Cardiac; Natriuretic Peptide, C-Type

2023
Atrial Fibrillation in Aging and Frail Mice: Modulation by Natriuretic Peptide Receptor C.
    Circulation. Arrhythmia and electrophysiology, 2021, Volume: 14, Issue:9

    [Figure: see text].

    Topics: Aging; Animals; Atrial Fibrillation; Biomarkers; Disease Models, Animal; Female; Heart Atria; Male; Mice; Natriuretic Peptide, C-Type

2021
C-type natriuretic peptide production by the human kidney is blunted in chronic heart failure.
    Clinical science (London, England : 1979), 2009, Oct-02, Volume: 118, Issue:1

    CNP (C-type natriuretic peptide) is a vasodilatory peptide produced by vascular endothelium and the human heart with a short half-life. CNP has been identified within the human kidney; however, few results are available on whether the human kidney is a systemic source of CNP. The aim of the present study was to establish whether CNP is secreted by the human kidney and if synthesis is blunted in CHF (chronic heart failure). A total of 20 male subjects (age, 57+/-2 years; mean+/-S.E.M.) undergoing CHF assessment (n=13) or investigation of paroxysmal supraventricular arrhythmia (normal left ventricular function in sinus rhythm during procedure) (n=7) were recruited. Renal CNP production was determined from concomitant plasma concentrations in the aorta and renal vein. When considering all subjects, a significant step-up in plasma CNP was found from the aorta to renal vein (3.0+/-0.3 compared with 8.3+/-2.4 pg/ml respectively; P=0.0045). The mean increase in CNP was 5.3+/-2.4 pg/ml (range, -0.9 to +45.3 pg/ml). In patients with CHF, the aortic concentration was 3.3+/-0.4 pg/ml compared with a renal vein concentration of 4.3+/-0.6 pg/ml (P=0.11). In those with normal left ventricular function, the respective values were 2.5+/-0.5 and 15.7+/-6.0 pg/ml (P=0.01). In conclusion, CNP is synthesized and secreted into the circulation by the normal human kidney, where it may have paracrine actions. Net renal secretion of CNP appears to be blunted in patients with CHF.

    Topics: Aged; Aorta; Atrial Fibrillation; Chronic Disease; Heart Failure; Humans; Kidney; Male; Middle Aged; Natriuretic Peptide, C-Type; Renal Veins; Ventricular Function, Left

2009