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Mechanisms of reflex bradycardia and hypotension by metabolites of arachidonic acid in the cat
Author(s) -
Hintze Thomas H.,
Kaley Gabor,
Panzenbeck Maret J.
Publication year - 1984
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.1476-5381.1984.tb16448.x
Subject(s) - bradycardia , arachidonic acid , reflex bradycardia , anesthesia , prostacyclin , reflex , medicine , heart rate , tachycardia , mean arterial pressure , atropine , prostaglandin , endocrinology , blood pressure , chemistry , biochemistry , enzyme
1 In the cat, intravenous injections of arachidonic acid or prostaglandin (PG)F 2α caused significant reductions in mean arterial pressure and heart rate which were eliminated or significantly lessened, respectively, by previous administration of indomethacin. The bradycardia to intravenous prostacyclin (PGI 2 ) was unaffected by indomethacin. 2 In cats with bilateral ligation of the carotid arteries to eliminate competition between systemic baroreflexes and cardiopulmonary reflexes, PGI 2 , PGF 2α and arachidonic acid caused significantly greater hypotension and bradycardia than in cats with intact carotid baroreflexes. 3 The bradycardia to PGI 2 , PGF 2α and arachidonic acid was eliminated by bilateral vagal section or atropine. 4 PGE 1 , PGE 2 and nitroprusside caused dose‐related falls in mean arterial pressure and a small tachycardia. 5 In a small group of cats (7 of 67) nitroprusside also caused a reduction in heart rate which was eliminated by indomethacin. 6 We conclude that the reflex bradycardia to PGF 2α , like that to arachidonic acid is, at least in part, the result of the stimulation of synthesis of another prostaglandin, most likely PGI 2 .