Bristow D R, Curtis N R, Suman-Chauhan N, Watling K J, Williams B J
Br J Pharmacol. 1987 Jan;90(1):211-7. doi: 10.1111/j.1476-5381.1987.tb16842.x.
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.
在仓鼠膀胱切片中检测速激肽刺激的肌醇磷脂水解。在存在锂以抑制肌醇单磷酸酶活性的情况下，P物质、伊列毒素及相关速激肽可诱导[3H] - 肌醇单磷酸积累出现大量、剂量依赖性增加。对P物质和伊列毒素的反应不受胆碱受体拮抗剂阿托品的拮抗。各种速激肽的效价顺序为：蛙皮素＞神经激肽A＞神经激肽B＞伊列毒素＞南美蛙皮素＞P物质＞P物质甲酯。合成类似物[p - Glu6, D - Pro9]SP(6 - 11)在刺激肌醇磷脂水解方面比其L - 脯氨酰立体异构体的效力强得多。这些结果表明，在仓鼠膀胱中，速激肽诱导的肌醇磷脂分解是通过SP - E型速激肽受体介导的，而非SP - P型。
