Fitts D A, Thunhorst R L, Simpson J B
Brain Res. 1985 Nov 25;348(1):118-24. doi: 10.1016/0006-8993(85)90367-1.
Infusions of 60 pmol/h atriopeptin II into the lateral ventricles stimulated urine flow in both normally hydrated and sodium depleted conscious rats without any increase in the excretion of sodium, potassium or total solutes. The urinary sodium concentration and osmolality both declined significantly. In addition to the renal effects, cerebroventricular infusions of 60 pmol/h atropeptin II reduced salt appetite in rats following depletion of sodium by combined treatment with furosemide diuresis and low sodium diet. Neither 60 nor 600 pmol/h doses had any effect on urine volume or concentration during intravenous infusions, so the effects appear to be mediated by the central nervous system (CNS). Atriopeptins may act through the CNS to facilitate reduction of extracellular volume in synergy with peripheral natriuresis: by increasing urine flow independently from natriuresis; and by restricting further expansion of extracellular volume by reducing salt appetite.
向正常水合和缺钠清醒大鼠的侧脑室以60皮摩尔/小时的速率输注心房肽II可刺激尿流,而钠、钾或总溶质的排泄量均未增加。尿钠浓度和渗透压均显著下降。除了对肾脏的影响外,向脑室输注60皮摩尔/小时的阿曲肽II可降低经速尿利尿和低钠饮食联合处理使钠耗竭后的大鼠的盐食欲。静脉输注时,60皮摩尔/小时和600皮摩尔/小时的剂量对尿量或尿浓缩均无影响,因此这些作用似乎是由中枢神经系统(CNS)介导的。心房肽可能通过中枢神经系统发挥作用,与外周排钠协同促进细胞外液量减少:通过独立于排钠增加尿流;以及通过降低盐食欲限制细胞外液量的进一步扩张。