{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Mesquita T"],"funding":["NHLBI NIH HHS"],"pagination":["45-60"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9083886"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["145(1)"],"pubmed_abstract":["Background
The ability to increase heart rate during exercise and other stressors is a key homeostatic feature of the sinoatrial node (SAN). When the physiological heart rate response is blunted, chronotropic incompetence limits exercise capacity, a common problem in patients with heart failure with preserved ejection fraction (HFpEF). Despite its clinical relevance, the mechanisms of chronotropic incompetence remain unknown.Methods
Dahl salt-sensitive rats fed a high-salt diet and C57Bl6 mice fed a high-fat diet and an inhibitor of constitutive nitric oxide synthase (Nω-nitro-L-arginine methyl ester [L-NAME]; 2-hit) were used as models of HFpEF. Myocardial infarction was created to induce HF with reduced ejection fraction. Rats and mice fed with a normal diet or those that"],"journal":["Circulation"],"pubmed_title":["Mechanisms of Sinoatrial Node Dysfunction in Heart Failure With Preserved Ejection Fraction."],"pmcid":["PMC9083886"],"funding_grant_id":["U01 HL141074","R01 HL142496","R01 HL126802","R01 HL147570","R01 HL135866"],"pubmed_authors":["Liang JA","Cingolani E","Goldhaber JI","Cho JH","Mesquita T","Zhang R","Lin YN","Sanchez L","Yu JK","Liu W","Trayanova NA"],"additional_accession":[]},"is_claimable":false,"name":"Mechanisms of Sinoatrial Node Dysfunction in Heart Failure With Preserved Ejection Fraction.","description":"Background
The ability to increase heart rate during exercise and other stressors is a key homeostatic feature of the sinoatrial node (SAN). When the physiological heart rate response is blunted, chronotropic incompetence limits exercise capacity, a common problem in patients with heart failure with preserved ejection fraction (HFpEF). Despite its clinical relevance, the mechanisms of chronotropic incompetence remain unknown.Methods
Dahl salt-sensitive rats fed a high-salt diet and C57Bl6 mice fed a high-fat diet and an inhibitor of constitutive nitric oxide synthase (Nω-nitro-L-arginine methyl ester [L-NAME]; 2-hit) were used as models of HFpEF. Myocardial infarction was created to induce HF with reduced ejection fraction. Rats and mice fed with a normal diet or those that","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Jan","modification":"2026-05-30T15:26:13.648Z","creation":"2025-04-04T10:01:51.821Z"},"accession":"S-EPMC9083886","cross_references":{"pubmed":["34905696"],"doi":["10.1161/CIRCULATIONAHA.121.054976","10.1161/circulationaha.121.054976"]}}