Prostacyclin (PGI2) Elicits Reflex Bradycardia in Dogs: Evidence for Vagal Mediation

Administration of the vasode-pressor prostaglandins, PGE1 and PGE2, and of nitroprusside, an agent whose direct vascular activity is similar to prostaglandins, resulted in a reduction in systemic arterial blood pressure accompanied by the expected reflex increase in heart rate. Injection of pros-tacyclin (PGI2) and the prostaglandin precursor, arachidonic acid, into the femoral vein, pulmonary artery, left atrium, and left ventricle of the dog elicited a fall in blood pressure and a concomitant reduction in heart rate in both open- and closed-chest anesthetized dogs. Bilateral vagal section eliminated the bradycardia thus establishing that the PGI2-induced change in heart rate is reflex in origin.