Mason D F, Medbak S, Rees L H
Br J Pharmacol. 1987 May;91(1):103-11. doi: 10.1111/j.1476-5381.1987.tb08988.x.
The effects of either hypotension induced by sodium nitroprusside or hexamethonium or hypertension produced by angiotensin II or noradrenaline on the circulating levels of methionine enkephalin ([Met]enkephalin)-like immunoreactivity (MLI), adrenaline and noradrenaline in anaesthetized greyhounds were examined. Nitroprusside infusions (200 and 400 micrograms min-1) induced a fall in blood pressure accompanied by significant rises in plasma MLI and catecholamine concentrations. Concomitant administration of a high dose of naloxone did not alter the fall in blood pressure produced by nitroprusside but was associated with greater rises in circulating MLI and catecholamines when compared to nitroprusside alone, suggesting that [Met]enkephalin is not involved in the hypotensive action of nitroprusside. Intravenous hexamethonium (2.5 mg kg-1) provoked a fall in blood pressure which was not associated with any changes in plasma MLI. However, it produced a fall in plasma noradrenaline and a rise in plasma adrenaline. Thus it appears that neural mechanisms are required, at least in part, for the release of MLI. Angiotensin II (1.25 micrograms kg-1 min-1) and noradrenaline (8 micrograms kg-1 min-1) infusions produced an elevation in blood pressure without altering the circulating MLI levels. Study of the molecular forms of circulating MLI, before and during hypotension, revealed that the large molecular weight enkephalin-containing peptides with approximate molecular sizes of 18kD and 8kD were the predominant forms both in the basal and stimulated states. It is concluded that circulating [Met]enkephalin is not involved in the tonic control of blood pressure but it may modulate catecholamine release following hypotension as part of the stress response.
研究了硝普钠或六甲铵诱导的低血压以及血管紧张素 II 或去甲肾上腺素引起的高血压对麻醉灵缇犬循环中蛋氨酸脑啡肽([Met]脑啡肽)样免疫反应性(MLI)、肾上腺素和去甲肾上腺素水平的影响。输注硝普钠(200 和 400 微克/分钟)导致血压下降,同时血浆 MLI 和儿茶酚胺浓度显著升高。与单独使用硝普钠相比,同时给予高剂量纳洛酮并未改变硝普钠引起的血压下降,但与循环中 MLI 和儿茶酚胺的更大升高相关,这表明 [Met]脑啡肽不参与硝普钠的降压作用。静脉注射六甲铵(2.5 毫克/千克)引起血压下降,这与血浆 MLI 的任何变化无关。然而,它导致血浆去甲肾上腺素下降和血浆肾上腺素升高。因此,似乎至少部分需要神经机制来释放 MLI。输注血管紧张素 II(1.25 微克/千克/分钟)和去甲肾上腺素(8 微克/千克/分钟)导致血压升高,而不改变循环中的 MLI 水平。对低血压前后循环 MLI 的分子形式研究表明,分子量约为 18kD 和 8kD 的含脑啡肽的大分子肽在基础状态和刺激状态下都是主要形式。得出的结论是,循环中的 [Met]脑啡肽不参与血压的紧张性控制,但它可能作为应激反应的一部分在低血压后调节儿茶酚胺的释放。