sb-269970 and Bradycardia

Although depression and cardiovascular diseases are related, the role of antidepressants such as fluoxetine (increasing serotonin levels) within cardiac regulation remains unclear. We aimed to determine whether fluoxetine modifies the pharmacological profile of serotonergic influence on vagal cardiac outflow. Rats were treated with fluoxetine (10 mg/kg per day; p.o.) for 14 days or equivalent volumes of drinking water (control group); then, they were pithed and prepared for vagal stimulation. Bradycardic responses were obtained by electrical stimulation of the vagal fibers (3, 6, and 9 Hz) or i.v. acetylcholine (ACh; 1, 5, and 10 μg/kg). The i.v. administration of 5-hydroxytryptamine (5-HT; 10 and 50 μg/kg) inhibited the vagally induced bradycardia. 5-CT (5-HT

Topics: Administration, Oral; Animals; Antidepressive Agents, Second-Generation; Bradycardia; Depression; Disease Models, Animal; Drug Evaluation, Preclinical; Fluoxetine; Heart; Heart Rate; Humans; Oxadiazoles; Phenols; Rats; Rats, Wistar; Receptor, Serotonin, 5-HT1D; Serotonin; Serotonin 5-HT1 Receptor Antagonists; Serotonin Receptor Agonists; Sulfonamides; Tryptamines; Vagus Nerve