Sezen S F, Kenigs V A, Kapusta D R
Department of Pharmacology and Experimental Therapeutics, Louisiana State University Medical Center, New Orleans, Louisiana, USA.
J Pharmacol Exp Ther. 1998 Oct;287(1):238-45.
Studies were performed in conscious Sprague-Dawley rats to characterize the changes in renal excretory function produced by activation of delta opioid systems. The intravenous infusion of 50 microgram/kg/min, BW373U86 (BW), a nonpeptide delta opioid receptor agonist, produced a significant increase in urine flow rate and urinary sodium excretion. The infusion of BW at a dose of 30 microgram/kg/min produced diuresis without affecting urinary sodium excretion. In contrast, BW did not alter either renal excretory parameter at a dose of 10 microgram/kg/min. The renal responses produced by BW occurred without changes in heart rate or mean arterial blood pressure. The diuretic and natriuretic responses produced by the i.v. infusion of BW (50 microgram/kg/min) were prevented by pretreatment of animals with the selective delta opioid receptor antagonist, naltrindole (1 mg/kg, i.v.). When administered alone, naltrindole (1 mg/kg, i.v.) failed to change any systemic cardiovascular or renal excretory parameter. In other groups of animals, the peripheral administration of the delta opioid receptor agonist, SNC80, also evoked a profound diuretic and natriuretic response (naltrindole sensitive) similar to that produced by BW. In contrast to these findings, the diuretic and natriuretic response produced by BW infusion (30 or 50 microgram/kg/min, i.v.) was abolished in rats having undergone chronic bilateral renal denervation. Together, these results demonstrate that the peripheral administration of BW373U86 or SNC80 produce marked diuretic and natriuretic responses in conscious Sprague-Dawley rats via a delta opioid receptor pathway and that intact renal nerves are required for mediating these responses. Although endogenous delta opioid systems do not appear to exert a tonic influence under basal conditions, these findings suggest that delta opioid pathways may evoke significant changes in renal excretory function under conditions in which these systems are activated.
在清醒的Sprague-Dawley大鼠中进行了研究,以表征δ阿片系统激活所产生的肾排泄功能变化。以50微克/千克/分钟的剂量静脉输注非肽类δ阿片受体激动剂BW373U86(BW),可使尿流率和尿钠排泄量显著增加。以30微克/千克/分钟的剂量输注BW可产生利尿作用,但不影响尿钠排泄。相比之下,以10微克/千克/分钟的剂量输注BW不会改变任何一项肾排泄参数。BW所产生的肾脏反应在心率或平均动脉血压无变化的情况下发生。静脉输注BW(50微克/千克/分钟)所产生的利尿和利钠反应可被用选择性δ阿片受体拮抗剂纳曲吲哚(1毫克/千克,静脉注射)预处理动物所阻断。单独给予纳曲吲哚(1毫克/千克,静脉注射)时,未能改变任何全身心血管或肾排泄参数。在其他几组动物中,外周给予δ阿片受体激动剂SNC80也会引发类似于BW所产生的深刻利尿和利钠反应(对纳曲吲哚敏感)。与这些发现相反,在经历慢性双侧肾去神经支配的大鼠中,BW输注(30或50微克/千克/分钟,静脉注射)所产生的利尿和利钠反应被消除。总之,这些结果表明,外周给予BW373U86或SNC80可通过δ阿片受体途径在清醒的Sprague-Dawley大鼠中产生显著的利尿和利钠反应,并且完整的肾神经是介导这些反应所必需的。尽管内源性δ阿片系统在基础条件下似乎未发挥紧张性影响,但这些发现表明,在这些系统被激活的情况下,δ阿片途径可能会引起肾排泄功能的显著变化。