Debska-Slizien A, Ho P, Drangova R, Baines A D
Department of Clinical Biochemistry, University of Toronto, Ontario, Canada.
Am J Physiol. 1994 Jun;266(6 Pt 2):F858-67. doi: 10.1152/ajprenal.1994.266.6.F858.
We examined the effect of endogenous dopamine production on Pi and citrate excretion by Wistar rats. Carbidopa (20-40 mumol/kg ip) decreased dopamine, Pi, and citrate excretion within 20 min (86%, 47%, and 38%, respectively); Pi reabsorption increased 11 +/- 4% (P = 0.03). The decreases were sustained for at least 18 h. 3-Hydroxybenzylhydrazine (45 mumol/kg ip) reduced Pi excretion 24%. Benserazide (40 mumol/kg ip and 0.1 mumol/min iv) reduced dopamine excretion (94%) and blocked the effect of carbidopa on Pi and citrate excretion. In isolated perfused kidneys benserazide, carbidopa, and 3-hydroxybenzylhydrazine all decreased Pi excretion. Dopamine (1 mumol/l) added to cortical minceates reduced brush-border membrane vesicle (BBMV) 32P uptake by 8% (P < 0.02) and amiloride-inhibitable 22Na uptake by 19%. Carbidopa added to minceates increased 32P uptake by 12%. Carbidopa pretreatment increased (75%) amiloride-sensitive 22Na uptake into BBMV of rats fed a high-salt diet. Uptake was not increased into BBMV from rats fed a low-salt diet. Carbidopa increased (17%) basolateral membrane Na(+)-K(+)-adenosinetriphosphatase (Na(+)-K(+)-ATPase) gradually over 4 h. Na(+)-K(+)-ATPase did not increase in rats fed a low-phosphorous diet, but did increase when dopa was added to the diet. Thus endogenous dopamine appears to directly control Na(+)-Pi and Na+/H+ transport and secondarily alter basolateral membrane Na(+)-K(+)-ATPase.
我们研究了内源性多巴胺生成对Wistar大鼠磷（Pi）和柠檬酸盐排泄的影响。卡比多巴（20 - 40 μmol/kg，腹腔注射）在20分钟内可降低多巴胺、Pi和柠檬酸盐的排泄（分别降低86%、47%和38%）；Pi重吸收增加11±4%（P = 0.03）。这些降低至少持续18小时。3 - 羟基苄肼（45 μmol/kg，腹腔注射）使Pi排泄减少24%。苄丝肼（40 μmol/kg，腹腔注射和0.1 μmol/min，静脉注射）降低多巴胺排泄（94%），并阻断卡比多巴对Pi和柠檬酸盐排泄的作用。在离体灌注肾中，苄丝肼、卡比多巴和3 - 羟基苄肼均降低Pi排泄。向皮质切碎组织中添加多巴胺（1 μmol/l）使刷状缘膜囊泡（BBMV）的32P摄取降低8%（P < 0.02），使阿米洛利可抑制的22Na摄取降低19%。向切碎组织中添加卡比多巴使32P摄取增加12%。卡比多巴预处理使高盐饮食大鼠的BBMV中阿米洛利敏感的22Na摄取增加（75%）。低盐饮食大鼠的BBMV摄取未增加。卡比多巴在4小时内逐渐使基底外侧膜钠钾腺苷三磷酸酶（Na(+)-K(+)-ATPase）增加（17%）。低磷饮食大鼠的Na(+)-K(+)-ATPase未增加，但在饮食中添加多巴时会增加。因此，内源性多巴胺似乎直接控制Na(+)-Pi和Na+/H+转运，并继而改变基底外侧膜Na(+)-K(+)-ATPase。
