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REFLEX BRADYCARDIA AND HYPOTENSION PRODUCED BY PROSTAGLANDIN F 2α IN THE CAT
Author(s) -
KOSS M.C.,
NAKANO J.
Publication year - 1976
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1976.tb07635.x
Subject(s) - bradycardia , heart rate , prostaglandin f2alpha , medicine , reflex bradycardia , anesthesia , blood pressure , atropine , aorta , chronotropic , pulmonary artery , cardiology , prostaglandin
1 Intravenous administration of prostaglandin F 2α results in a dose‐dependent increase in pulmonary arterial pressure, decrease in systemic arterial pressure and a delayed bradycardia. Pulmonary vasoconstriction was observed at doses as low as 0.1 and 0.3 μg/kg. The systemic depressor and heart rate lowering effects were observed at 1 μg/kg doses and above. 2 A moderate bradycardia was still observed after atropine blockade but was abolished following bilateral vagotomy. Neither of these procedures affected the pulmonary vascular response. 3 Injections of submaximal doses of prostaglandin F 2α (1–4 μg/kg) produced a greater and longer lasting bradycardia when injected into the left atrium than was observed following intravenous administration. In addition the latency of onset was much shorter following left atrial injection. These doses resulted in no change in heart rate and a minimal hypotension when injected into the brachiocephalic artery or into the aortic arch. 4 Small doses of prostaglandin F 2α administered at the level of the origin of the coronary arteries produced marked decreases in heart rate and blood pressure whereas no change occurred following injection of the same amount into the ascending aorta at more distal sites. 5 These results suggest that prostaglandin F 2α produces bradycardia and hypotension in the cat by activating ‘receptors’ located in the left heart or by acting on structures perfused by means of the coronary arteries.