Kau M M, Huang W C
National Taipei College of Nursing, Taiwan, ROC.
Chin J Physiol. 1991;34(3):317-31.
Our previous study demonstrated that acutely or chronically unilateral renal denervation did not blunt intravenous ANF--induced hypotensive and ipsilateral renal effects. The present study was further to examine the permissive role of renal nerve and dopamine in the renal action of ANF. Experiments were conducted on anesthetized rats with either acute unilateral ureter ligation (n = 8), reserpine pretreatment (10 mg/kg, n = 7), mechanically controlled renal arterial pressure (n = 8) or blockade of dopamine D1 receptors by SCH23390 (n = 8, 0.8 micrograms/kg.min). The arterial blood pressure and renal clearance responses to intravenous (0.30-0.45 micrograms/kg.min) or intrarenal (0.10-0.15 micrograms/kg.min) infusion of ANF were measured. The results showed that unilateral ligation of the ureter to physiologically inhibit the contralateral renal efferent nerve activity did not alter the depressor, diuretic and natriuretic effects of ANF. Reserpine pretreatment blunted the diuretic and natriuretic response to intravenous administration of ANF. However, ANF-induced diuresis and natriuresis was persistently observed in both kidneys of rats with the left renal arterial pressure being controlled at a level comparable to that seen in the reserpine-pretreated group. Blockade of intrarenal dopamine D1 receptors by SCH23390 completely abolished the diuretic and natriuretic response to intrarenal infusion of ANF. These results support the notion that the diuretic and natriuretic effect of ANF is not resulted from a decrease in renal sympathetic efferent nerve activity, and further indicate that a mechanism associated with activation of the renal dopamine D1 receptors mediates the renal effect of ANF in rats.
我们之前的研究表明,急性或慢性单侧肾去神经支配并不会减弱静脉注射心房钠尿肽(ANF)所诱导的降压作用及同侧肾脏效应。本研究进一步探讨肾神经和多巴胺在ANF肾脏作用中的允许作用。实验在麻醉大鼠上进行,分别采用急性单侧输尿管结扎(n = 8)、利血平预处理(10 mg/kg,n = 7)、机械控制肾动脉血压(n = 8)或用SCH23390阻断多巴胺D1受体(n = 8,0.8微克/千克·分钟)。测量静脉注射(0.30 - 0.45微克/千克·分钟)或肾内注射(0.10 - 0.15微克/千克·分钟)ANF后的动脉血压和肾脏清除率反应。结果显示,单侧输尿管结扎以生理方式抑制对侧肾传出神经活动,并未改变ANF的降压、利尿和排钠作用。利血平预处理减弱了静脉注射ANF后的利尿和排钠反应。然而,在左肾动脉血压控制在与利血平预处理组相当水平的大鼠双肾中,持续观察到ANF诱导的利尿和排钠作用。用SCH23390阻断肾内多巴胺D1受体完全消除了肾内注射ANF后的利尿和排钠反应。这些结果支持以下观点:ANF的利尿和排钠作用并非源于肾交感传出神经活动的降低,并且进一步表明,与肾多巴胺D1受体激活相关的机制介导了ANF在大鼠中的肾脏作用。