Qian Y, Advenier C, Naline E, Bellamy J F, Emonds-Alt X
Faculté de Médecine Paris-Ouest, Paris, France.
Fundam Clin Pharmacol. 1994;8(1):71-5. doi: 10.1111/j.1472-8206.1994.tb00781.x.
Neuropeptide gamma (NP gamma) induced a contractile response of the human isolated bronchus which was potentiated by the neutral endopeptidase inhibitor, phosphoramidon, but was not modified by atropine and indomethacin. NP gamma was 3.31-fold more potent than NKA. Contractile response curves to NP gamma were shifted to the right and maximal responses reduced by the non-peptide NK2-receptor antagonist, SR 48968. The pKB of SR 48968 (8.94 +/- 0.18, n = 15), calculated according to Kenakin (1987) was very close to that reported for [Nle10]-NKA (4-10), a specific agonist of neurokinin NK2-receptors (8.86 +/- 0.13, n = 13), suggesting that the contractile effects of NP gamma on the human isolated bronchus were mediated through NK2A-receptors.
神经肽γ（NPγ）可引起人离体支气管的收缩反应，中性内肽酶抑制剂磷酰胺素可增强该反应，但阿托品和吲哚美辛对其无影响。NPγ的效力比神经激肽A（NKA）高3.31倍。非肽类NK2受体拮抗剂SR 48968可使NPγ的收缩反应曲线右移，最大反应降低。根据凯纳金（1987年）计算，SR 48968的pKB值（8.94±0.18，n = 15）与神经激肽NK2受体特异性激动剂[异亮氨酸10]-NKA（4-10）报道的pKB值（8.86±0.13，n = 13）非常接近，这表明NPγ对人离体支气管的收缩作用是通过NK2A受体介导的。
