ENDOGENOUS RENAL DOPAMINE PRODUCTION REGULATES PHOSPHATE EXCRETION

We examined the effect of endogenous dopamine production on P-i and citrate excretion by Wistar rats. Carbidopa (20-40 mu mol/kg ip) decreased dopamine, P-i, and citrate excretion within 20 min (86%, 47%, and 38%, respectively); P-i reabsorption increased 11 +/- 4% (P = 0.03). The decreases were sustained for at least 18 h. 3-Hydroxybenzylhydrazine (45 mu mol/kg ip) reduced P-i excretion 24%. Benserazide (40 mu mol/kg ip and 0.1 mu mol/min iv) reduced dopamine excretion (94%) and blocked the effect of carbidopa on P-i and citrate excretion. In isolated perfused kidneys benserazide, carbidopa, and 3-hydroxybenzylhydrazine all decreased P-i excretion. Dopamine (1 mu mol/l) added to cortical minceates reduced brush-border membrane vesicle (BBMV) P-32 uptake by 8% (P < 0.02) and amiloride-inhibitable Na-22 uptake by 19%. Carbidopa added to minceates increased P-32 uptake by 12%. Carbidopa pretreatment increased (75%) amiloride-sensitive Na-22 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+-P-i and Na+/H+ transport and secondarily alter basolateral membrane Na+-K+-ATPase.