Kérouac R, St-Pierre S, Rioux F
Neuropeptides. 1982 Dec;3(2):145-57. doi: 10.1016/0143-4179(82)90010-5.
Intravenous injections of neurotensin (NT) (0.5, 1 and 2 nmoles kg-1) evoked dose-dependent increases in histaminemia and hematocrit, and marked hypotensive effect, in anesthetized rats. The increase of plasma histamine was rapid in onset (within sec), peak plasma histamine being reached in less than 2 min. The decline of plasma histamine was gradual and almost complete 15 min after injection of NT. The hematocrit increased slowly, maximum values being obtained 5-10 min after injection of NT, and it persisted throughout the period of observation. The hypotensive effect of NT was rapid in onset and of prolonged duration. Compound 48/80, a well known histamine liberator and mast cell depletor, produced variations of blood pressure, of hematocrit and of plasma histamine very similar to those elicited by NT. Pretreatment of rats with cromoglycate, a well known mast cell stabilizer, or with dexamethasone, inhibited markedly the changes of histaminemia, of hematocrit and of blood pressure evoked by NT and compound 48/80. The results clearly suggest that the effects of NT on blood pressure and on vascular permeability in rats are mediated to some extent by mast cell histamine. Hexamethonium, a ganglion blocker, inhibited slightly the effect of NT on histaminemia but it did not block NT-induced changes of hematocrit. However, the hypotensive effect of NT was severely blocked in hexamethonium-treated rats. These results were interpretated as an indication that hexamethonium prevents NT-induced hypotension not merely by reducing the mobilization of mast cell histamine by NT but most likely by interfering with the mechanism by which NT and/or its mast cell mediators produce their effects on blood pressure.
静脉注射神经降压素（NT）（0.5、1和2纳摩尔/千克）可使麻醉大鼠的组胺血症和血细胞比容呈剂量依赖性增加，并产生明显的降压作用。血浆组胺的升高起效迅速（数秒内），不到2分钟即可达到血浆组胺峰值。注射NT后15分钟，血浆组胺逐渐下降且几乎完全消失。血细胞比容缓慢升高，注射NT后5 - 10分钟达到最大值，并在整个观察期持续存在。NT的降压作用起效迅速且持续时间长。化合物48/80是一种著名的组胺释放剂和肥大细胞脱颗粒剂，其引起的血压、血细胞比容和血浆组胺变化与NT引起的非常相似。用著名的肥大细胞稳定剂色甘酸或地塞米松对大鼠进行预处理，可显著抑制NT和化合物48/80引起的组胺血症、血细胞比容和血压变化。结果清楚地表明，NT对大鼠血压和血管通透性的影响在一定程度上是由肥大细胞组胺介导的。神经节阻断剂六甲铵略微抑制了NT对组胺血症的作用，但并未阻断NT引起的血细胞比容变化。然而，在六甲铵处理的大鼠中，NT的降压作用被严重阻断。这些结果被解释为表明六甲铵预防NT诱导的低血压不仅是通过减少NT对肥大细胞组胺的动员，而且很可能是通过干扰NT和/或其肥大细胞介质对血压产生作用的机制。
