Abstract
Tachykinin-stimulated inositol phospholipid hydrolysis was examined in slices of hamster urinary bladder. In the presence of lithium, to inhibit inositol monophosphatase activity, substance P, eledoisin and related tachykinins induced large, dose-dependent increases in [3H]-inositol monophosphate accumulation. The responses to substance P and eledoisin were not antagonized by the cholinoceptor antagonist, atropine. The rank order of potency for various tachykinins was kassinin greater than neurokinin A greater than neurokinin B greater than eledoisin greater than physaelamin greater than substance P greater than substance P methyl ester. The synthetic analogue [p-Glu6, D-Pro9]SP (6-11) was considerably more potent than its L-prolyl stereoisomer at stimulating inositol phospholipid hydrolysis. These results suggest that in the hamster urinary bladder, tachykinin-induced inositol phospholipid breakdown is mediated via tachykinin receptors of the SP-E type, as opposed to the SP-P type.
MeSH Terms
Animals
Atropine/pharmacology
Carbachol/antagonists & inhibitors
Cricetinae
Hydrolysis
In Vitro Techniques
Inositol Phosphates/metabolism
Mesocricetus
Nerve Tissue Proteins/pharmacology
Receptors, Neurotransmitter/physiology
Receptors, Tachykinin
Sugar Phosphates/metabolism
Urinary Bladder/drug effects,metabolism
Chemicals
Inositol Phosphates
Nerve Tissue Proteins
Receptors, Neurotransmitter
Receptors, Tachykinin
Sugar Phosphates
Atropine
Carbachol
Authors & Affiliations
5 authors, click to expand affiliations / ORCID
Bristow D R
Curtis N R
Suman-Chauhan N
Watling K J
Williams B J
References (14)
14 references, click to expand
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