Atrial natriuretic peptide (ANP) plays a pivotal role in the regulation of the cardiovascular system. The ANP level increases during atrial fibrillation (AF), suggesting that AF may provoke ANP secretion, but its potential mechanism is still unclear. In the present study, the potential mechanisms of rapid atrial pacing (RAP) regulating ANP secretion was explored. Rabbits were subjected to burst RAP, ANP secretion increased whereas cyclic guanosine monophosphate (cGMP) concentrations decreased during RAP. The p-Akt and p-GSK-3β levels decreased in atrial tissues. Natriuretic peptide receptor A (NPR-A) protein and particulate guanylate cyclase (PGC) activity were detected. The sensitivity of NPR-A to ANP decreased, leading to the decrease of PGC activity. Also, the isolated atrial perfusion system were made in the rabbit model, cGMP was shown to inhibit ANP secretion, and the Akt inhibitor LY294002 (LY) and GSK-3β inhibitor SB216763 (SB) attenuated the inhibitory effects of cGMP on ANP secretion and enhanced the inhibitory effects of cGMP on atrial dynamics. In conclusion, NPR-A interacts with ANP to regulate PGC expression, and influence the expression of cGMP during RAP, which involves in the Akt/GSK-3β signaling pathway. From the aforementioned points we conclude that cGMP regulates ANP secretion by the Akt/GSK-3β signaling pathway during atrial pacing.
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http://dx.doi.org/10.3389/fphys.2022.861981 | DOI Listing |
Cells
January 2025
Institute of Anatomy & Cell Biology, Faculty of Medicine, Justus-Liebig-University, Aulweg 123, 35392 Giessen, Germany.
Vascular smooth muscle cell (SMC) relaxation by guanylyl cyclases (GCs) and cGMP is mediated by NO and its receptor soluble GC (sGC) or natriuretic peptides (NPs) ANP/BNP and CNP with the receptors GC-A and GC-B, respectively. It is commonly accepted that cultured SMCs differ from those in intact vessels. Nevertheless, cell culture often remains the first step for signaling investigations and drug testing.
View Article and Find Full Text PDFClin Chem
January 2025
Division of Maternal-Fetal-Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, United States.
Background: Genetic screening has advanced from prenatal cell-free DNA (cfDNA) screening for aneuploidies (cfDNA-ANP) to single-gene disorders (cfDNA-SGD). Clinical validation studies have been promising in pregnancies with anomalies but are limited in the general population.
Methods: Chart review and laboratory data identified pregnancies with cfDNA-SGD screening for 25 autosomal dominant conditions at our academic center.
Mol Biol Rep
December 2024
Department of Physiology, School of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.
Background: The role of 1,25-dihydroxyvitamin-D3 (VitD) and sirtuin-1 (SIRT1) in mitigating pathological cardiac remodeling is well recognized. However, the potential for SIRT1 to mediate the inhibitory effects of VitD on angiotensin II (Ang II) -induced hypertrophy in H9c2 cardiomyoblasts remains unclear.
Methods: H9c2 cardiomyoblasts were exposed to Ang II or a combination of VitD and Ang II, both in the absence and presence of SIRT1-specific siRNA.
Zhongguo Zhong Yao Za Zhi
October 2024
Institute of Basic Medical Sciences of Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing Key Laboratory of Chinese Materia Pharmacology, National Clinical Research Center of Traditional Chinese Medicine for Cardiovascular Diseases Beijing 100091, China Heilongjiang University of Chinese Medicine Harbin 150040, China.
To explore the regulation of vasodilatory function in rats with post-infarction heart failure by salvianolic acid B(Sal-B) based on the mechanosensitive ion channel, namely Piezo1. A post-infarction heart failure model of rats was prepared by ligation of the left anterior descending coronary artery. After successful modeling, the rats were randomly divided into the model group, Sal-B group(0.
View Article and Find Full Text PDFJ Cell Mol Med
December 2024
Inserm, CHU Lille, Institut Pasteur de Lille, U1167-RID-AGE, Université de Lille, Lille, France.
Chronic pressure overload induces adverse cardiac remodelling characterised by left ventricular (LV) hypertrophy and fibrosis, leading to heart failure (HF). Identification of new biomarkers for adverse cardiac remodelling enables us to better understand this process and, consequently, to prevent HF. We recently identified clusterin (CLU) as a biomarker of cardiac remodelling and HF after myocardial infarction.
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