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Mediation of bradykinin‐induced contraction in canine veins via thromboxane/prostaglandin endoperoxide receptor activation
Author(s) -
Aksoy Mark O.,
Harakal Concetta,
Smith J. Bryan,
Stewart Gwendolyn J.,
Zerweck Charles R.
Publication year - 1990
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.1476-5381.1990.tb12950.x
Subject(s) - bradykinin , chemistry , contraction (grammar) , endocrinology , medicine , thromboxane , prostaglandin , thromboxane a2 , vasoconstriction , receptor , prostaglandin h2 , prostacyclin , pharmacology , biochemistry , platelet
1 Canine jugular and femoral veins were studied to determine the possible importance of thromboxane (TXA 2 ) and prostaglandin endoperoxides (prostaglandin H 2 , PGH 2 ) in mediating bradykinin(BK)‐induced contraction. 2 Isolated vein rings incubated in modified Krebs solution contracted to TXA 2 /PGH 2 analogs SQ26655 and U44069 with potency of contraction exceeding that for BK. The potency ranking for both veins was SQ26655 > U44069 > BK > PGF 2α > TXB 2 > PGD 2 . 3 The cyclo‐oxygenase inhibitors indomethacin (3 × 10 −7 m ) and flufenamic acid (10 −5 m ) reduced BK contractions without affecting those induced by noradrenaline (NA). 4 TXA 2 /PGH 2 receptor antagonists SQ29548 (10 −8 m ) and BM13177 (10 −6 m ) strongly inhibited BK‐induced tension. The action of antagonists was reversible with negligible influence on NA‐elicited contraction. Selective removal of endothelium had no effect on BK‐induced contraction or the action of the antagonists. 5 The thromboxane synthase inhibitors dazoxiben (10 −4 m ) and CGS 12970 (10 −5 m ) had no significant inhibitory effect on BK‐induced tension. 6 These results suggest that in canine jugular and femoral vein, the action of BK is largely dependent upon stimulation of the cyclo‐oxygenase pathway to produce PGH 2 and possibly TXA 2 , which can activate a smooth muscle TXA 2 /PGH 2 receptor to elicit vasoconstriction.