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| http://dx.doi.org/10.1136/jmg.40.1.74 | DOI Listing |
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A Novel Method for Measurement of Cardiovascular Responses to Lower Body Negative Pressure in the Awake Instrumented Rat.
Am J Physiol Heart Circ Physiol
January 2025
Department of Pharmacology, Physiology and Neurobiology, University of Cincinnati College of Medicine, Cincinnati, OH.
Lower body negative pressure (LBNP) has been used for decades in humans to model arterial baroreceptor unloading and represents a powerful tool for evaluating cardiovascular responses to orthostatic challenge. However, LBNP studies in animals have been limited to conditions of anesthesia or sedation, where cardiovascular reflexes are altered. Given the consequent uncertainties, the usefulness of LBNP studies in these preclinical models has been severely hampered.
View Article and Find Full Text PDFPrenatal dexamethasone programs autonomic dysregulation in female rats.
Am J Physiol Heart Circ Physiol
February 2025
Department of Basic Medical Sciences, University of Arizona College of Medicine, Phoenix, Arizona, United States.
Autonomic dysfunction is associated with cardiovascular and neurological diseases, including hypertension, heart failure, anxiety, and stress-related disorders. Prior studies demonstrated that late gestation exposure to dexamethasone (DEX) resulted in female-biased increases in stress-responsive mean arterial pressure (MAP) and heart rate (HR), suggesting a role for glucocorticoid-mediated programming of autonomic dysfunction. The present study investigated the influence of sympathetic (SYM) or parasympathetic (PS) blockade on cardiovascular function in male and female rat offspring of mothers injected with DEX in utero [ (GD) -].
View Article and Find Full Text PDFPrognostic value of β1 adrenergic receptor autoantibodies for microvascular obstruction in patients with STEMI with Post-PCI: A prospective cohort study.
J Transl Autoimmun
December 2024
Department of Cardiology, Cardiovascular Centre, Beijing Friendship Hospital, Capital Medical University, 95 Yong'an Road, Xicheng District, Beijing, 100050, China.
Backgrounds: Coronary microvascular obstruction (MVO) frequently occurs in patients with ST-segment elevation myocardial infarction (STEMI) following percutaneous coronary intervention (PCI), leading to poor prognosis. β adrenergic receptor autoantibodies (β-AA) are present in various cardiovascular diseases and correlate with cardiac damage and dysfunction. However, whether β-AA is associated with the occurrence of MVO in patients with STEMI after PCI remains unclear.
View Article and Find Full Text PDFNephro- and Cardiotoxic Effects of Etoricoxib: Insights into Arachidonic Acid Metabolism and Beta-Adrenergic Receptor Expression in Experimental Mice.
Pharmaceuticals (Basel)
October 2024
Department of Physiology, Faculty of Medicine, King Abdulaziz University, Jeddah 21589, Saudi Arabia.
Etoricoxib is a widely used anti-inflammatory drug, but its safety profile concerning cardiovascular and renal health remains inadequately explored. This study aimed to assess the nephro- and cardiotoxic effects of etoricoxib in a murine model, with a focus on its impact on arachidonic acid-metabolizing enzymes and beta-adrenergic receptors associated with drug-induced toxicity. Thirty-five mice were randomly assigned to five groups: control, low-dose etoricoxib, high-dose etoricoxib, low-dose celecoxib, and high-dose celecoxib (a well-known nephro- and cardiotoxic NSAID).
View Article and Find Full Text PDFElectroacupuncture alleviates acute myocardial ischemic injury in mice by regulating the β adrenergic receptor and post-receptor protein kinase A signaling pathway.
Acupunct Med
December 2024
Institute of Acupuncture and Meridian, Anhui University of Chinese Medicine, Hefei, China.
Objective: To determine the effect of electroacupuncture (EA) on β-adrenergic receptor (β-AR) and post-receptor protein kinase A (PKA) signaling pathway after acute myocardial ischemia (MI).
Methods: An MI model was established by ligating the left anterior descending coronary artery of wild-type (WT) C57/BL and β-AR mice (heterozygous for β-AR gene deletion). EA treatment was administered at HT5-HT7 or LU9-LU8.
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