{"title":"多巴胺在残肾对甲状旁腺激素过度磷酸化反应中的作用。","authors":"J Isaac, T J Berndt, F G Knox","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>The remnant kidney (RK) exhibits an exaggerated phosphaturic response to parathyroid hormone (PTH) infusion. Increased urinary dopamine synthesis per nephron has been demonstrated in the remnant kidney, and dopamine infusion is phosphaturic. Therefore, the role of dopamine in the exaggerated phosphaturic response to PTH infusion in the RK was evaluated. To obtain the RK model, Sprague-Dawley rats were anesthetized and subjected to right nephrectomy as well as surgical ablation of the left renal poles. Sham surgery was performed in the other groups of rats. Four weeks later, acute experiments were performed in these animals. Two hours after thyroparathyroidectomy, a control clearance was taken. Subsequently, PTH (33 U/kg bolus, 1 U/kg/min) was infused for 60 minutes, followed by a 30-minute experimental clearance. In the rats with an RK, the increase in the fractional excretion of phosphate (FEPi) in response to PTH infusion was (delta 38.5% +/- 4.2%, n = 12). In an additional group of rats with an RK, the specific DA-1 receptor antagonist (SCH 23390, 25 micrograms/kg/min) was infused for 30 minutes, a control clearance was taken, and then PTH was infused. Infusion of SCH 23390 significantly blunted the phosphaturic response to PTH (FEPi, delta 24.0% +/- 7.7%, n = 7). In contrast, the phosphaturic response to PTH was similar in the rats that underwent sham surgery in the presence (delta FEPi, 25.4% +/- 1.6%, n = 5) and absence of infusion of SCH 23390 (delta FEPi 24.7 +/- 3.1%, n = 6).(ABSTRACT TRUNCATED AT 250 WORDS)</p>","PeriodicalId":23085,"journal":{"name":"The Journal of laboratory and clinical medicine","volume":"126 5","pages":"470-3"},"PeriodicalIF":0.0000,"publicationDate":"1995-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Role of dopamine in the exaggerated phosphaturic response to parathyroid hormone in the remnant kidney.\",\"authors\":\"J Isaac, T J Berndt, F G Knox\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The remnant kidney (RK) exhibits an exaggerated phosphaturic response to parathyroid hormone (PTH) infusion. Increased urinary dopamine synthesis per nephron has been demonstrated in the remnant kidney, and dopamine infusion is phosphaturic. Therefore, the role of dopamine in the exaggerated phosphaturic response to PTH infusion in the RK was evaluated. To obtain the RK model, Sprague-Dawley rats were anesthetized and subjected to right nephrectomy as well as surgical ablation of the left renal poles. Sham surgery was performed in the other groups of rats. Four weeks later, acute experiments were performed in these animals. Two hours after thyroparathyroidectomy, a control clearance was taken. Subsequently, PTH (33 U/kg bolus, 1 U/kg/min) was infused for 60 minutes, followed by a 30-minute experimental clearance. In the rats with an RK, the increase in the fractional excretion of phosphate (FEPi) in response to PTH infusion was (delta 38.5% +/- 4.2%, n = 12). In an additional group of rats with an RK, the specific DA-1 receptor antagonist (SCH 23390, 25 micrograms/kg/min) was infused for 30 minutes, a control clearance was taken, and then PTH was infused. Infusion of SCH 23390 significantly blunted the phosphaturic response to PTH (FEPi, delta 24.0% +/- 7.7%, n = 7). In contrast, the phosphaturic response to PTH was similar in the rats that underwent sham surgery in the presence (delta FEPi, 25.4% +/- 1.6%, n = 5) and absence of infusion of SCH 23390 (delta FEPi 24.7 +/- 3.1%, n = 6).(ABSTRACT TRUNCATED AT 250 WORDS)</p>\",\"PeriodicalId\":23085,\"journal\":{\"name\":\"The Journal of laboratory and clinical medicine\",\"volume\":\"126 5\",\"pages\":\"470-3\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1995-11-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"The Journal of laboratory and clinical medicine\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"The Journal of laboratory and clinical medicine","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
摘要
残肾(RK)对甲状旁腺激素(PTH)输注表现出夸张的磷化反应。在残肾中,每肾元尿多巴胺合成增加,多巴胺输注是磷化的。因此,我们评估了多巴胺在RK对PTH输注的过度磷酸化反应中的作用。为了获得RK模型,Sprague-Dawley大鼠麻醉后行右肾切除术和左肾极手术消融。其余各组大鼠均行假手术。4周后,对这些动物进行急性实验。甲状旁腺切除术后2小时,进行对照清除率测定。随后,PTH (33 U/kg丸,1 U/kg/min)输注60分钟,然后30分钟的实验间隙。在RK大鼠中,PTH输注后磷酸盐(FEPi)分数排泄增加(δ 38.5% +/- 4.2%, n = 12)。在另一组RK大鼠中,注射特异性DA-1受体拮抗剂(sch23390, 25微克/千克/分钟)30分钟,进行对照清除,然后注射甲状肾上腺素(PTH)。注射SCH 23390显著减弱了PTH的磷酸化反应(FEPi, δ 24.0% +/- 7.7%, n = 7)。相比之下,在假手术中注射SCH 23390 (δ FEPi, 25.4% +/- 1.6%, n = 5)和不注射SCH 23390 (δ FEPi 24.7 +/- 3.1%, n = 6)的大鼠对PTH的磷酸化反应相似。
Role of dopamine in the exaggerated phosphaturic response to parathyroid hormone in the remnant kidney.
The remnant kidney (RK) exhibits an exaggerated phosphaturic response to parathyroid hormone (PTH) infusion. Increased urinary dopamine synthesis per nephron has been demonstrated in the remnant kidney, and dopamine infusion is phosphaturic. Therefore, the role of dopamine in the exaggerated phosphaturic response to PTH infusion in the RK was evaluated. To obtain the RK model, Sprague-Dawley rats were anesthetized and subjected to right nephrectomy as well as surgical ablation of the left renal poles. Sham surgery was performed in the other groups of rats. Four weeks later, acute experiments were performed in these animals. Two hours after thyroparathyroidectomy, a control clearance was taken. Subsequently, PTH (33 U/kg bolus, 1 U/kg/min) was infused for 60 minutes, followed by a 30-minute experimental clearance. In the rats with an RK, the increase in the fractional excretion of phosphate (FEPi) in response to PTH infusion was (delta 38.5% +/- 4.2%, n = 12). In an additional group of rats with an RK, the specific DA-1 receptor antagonist (SCH 23390, 25 micrograms/kg/min) was infused for 30 minutes, a control clearance was taken, and then PTH was infused. Infusion of SCH 23390 significantly blunted the phosphaturic response to PTH (FEPi, delta 24.0% +/- 7.7%, n = 7). In contrast, the phosphaturic response to PTH was similar in the rats that underwent sham surgery in the presence (delta FEPi, 25.4% +/- 1.6%, n = 5) and absence of infusion of SCH 23390 (delta FEPi 24.7 +/- 3.1%, n = 6).(ABSTRACT TRUNCATED AT 250 WORDS)