Chen M, Lee J, Huang B S, Grekin R J, Malvin R L
Department of Physiology, University of Michigan, Ann Arbor.
Proc Soc Exp Biol Med. 1989 Jul;191(3):299-303. doi: 10.3181/00379727-191-42924.
In order to determine whether the activity of central alpha 2-adrenergic and opioid receptors influence plasma atrial natriuretic peptide (ANP) levels, clonidine and morphine were infused into the lateral cerebral ventricle for 45 min in anesthetized Sprague-Dawley rats. The central administration of a low dose of clonidine (10 ng/min) caused a significant increase in plasma ANP without changing arterial blood pressure or central venous pressure. Pretreatment with yohimbine (5 micrograms/min) completely blocked the effect of clonidine. Central infusion of morphine (100 ng/min) also elevated plasma ANP levels and naloxone (5 micrograms/min) blunted this effect. Intravenous infusion of the same dose of clonidine or morphine did not affect plasma ANP levels. Moreover, the effect of clonidine on plasma ANP was partially blocked by pretreatment with naloxone (5 micrograms/min). These results suggest that central alpha 2-adrenergic and opioid receptors may be involved in ANP secretion.
为了确定中枢α2 - 肾上腺素能受体和阿片受体的活性是否影响血浆心钠素(ANP)水平,在麻醉的斯普拉 - 道利大鼠的侧脑室内注入可乐定和吗啡45分钟。低剂量可乐定(10纳克/分钟)的中枢给药导致血浆ANP显著增加,而不改变动脉血压或中心静脉压。育亨宾(5微克/分钟)预处理完全阻断了可乐定的作用。中枢注入吗啡(100纳克/分钟)也升高了血浆ANP水平,而纳洛酮(5微克/分钟)减弱了这种作用。静脉内注入相同剂量的可乐定或吗啡不影响血浆ANP水平。此外,纳洛酮(5微克/分钟)预处理部分阻断了可乐定对血浆ANP的作用。这些结果表明中枢α2 - 肾上腺素能受体和阿片受体可能参与ANP的分泌。