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Characterization of tachykinin receptors in isolated basilar arteries of guinea‐pig
Author(s) -
Edvinsson Lars,
Jansen Inger
Publication year - 1987
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.1476-5381.1987.tb11205.x
Subject(s) - eledoisin , substance p , neurokinin a , schild regression , neurokinin b , tachykinin receptor , agonist , chemistry , basilar artery , receptor , medicine , endocrinology , guinea pig , serotonin , neuropeptide , biology , biochemistry
1 In circular lengths cut from the basilar artery of guinea‐pig (0.2‐0.3 mm o.d.) relaxations induced by substance P and neurokinin A were highly susceptible to mechanical damage of the endothelium by rubbing. The precontraction induced by prostaglandin F 2α but not that of 124 m m potassium was reduced considerably by the rubbing procedure. 2 Concentration‐dependent relaxations were evoked by tachykinin agonists in the following order of potency: substance P = physalaemin > neurokinin A > eledoisin. Physalaemin was, however, a partial agonist, giving only half the maximum relaxation as compared to the other tachykinins. 3 The two putative tachykinin receptor antagonists, spantide ([ d ‐Arg 1 , d ‐Trp 7,9 , d ‐Leu 11 ] substance P) and [ d ‐Pro 2 , d ‐Trp 7,9 ] substance P, shifted the concentration‐dependent relaxations of substance P to the right in a parallel manner. Calculation of pA 2 values and Schild plot analysis revealed pA 2 values of 7.4–7.6 for spantide and 6.9‐7.0 for [ d ‐Pro 2 , d ‐Trp 7,9 ] substance P, irrespective of whether substance P or neurokinin A was used as agonist. The pA 2 values and the Schild plot analysis suggest a specific interaction between tachykinin agonists and antagonists that follow a simple bimolecular process. 4 The results suggest the presence of tachykinin receptors of the ‘SP‐P’ type in guinea‐pig basilar arteries which, for induction of relaxation, involves the release of an endothelium‐derived relaxing factor.