EFFECT OF NOREPINEPHRINE ON CELLULAR SODIUM-TRANSPORT IN AMBYSTOMA KIDNEY PROXIMAL TUBULE

The effect of norepinephrine (NE) on mechanisms of cellular Na+ transport in the isolated, perfused proximal tubule of Ambystoma tigrinum was examined. Single-barreled voltage and ion-selective microelectrodes were used to determine basolateral (V-1), luminal (V-2), and transepithelial (V-3) membrane potentials and intracellular Na+ activity (alpha(Nai)). In CO2/HCO3- control solution, addition of NE (10(-6) M) to the bath caused depolarizations of V-1, V-2, and V-3 and decreased alpha(Nai). These effects were mimicked by isoproterenol and inhibited by propranolol. Addition of NE in the absence of luminal Na+ and substrates did not cause any changes in V-1, V-2, V-3, Or alpha(Nai). NE did not affect the changes in membrane potential difference (PD) or alpha(Nai) caused by removal and readdition of luminal substrates Nat. To study the effect of NE on Na-K-adenosinetriphosphatase (Na-K-ATPase), the pump was inhibited by external K+ removal and then reactivated by readdition of 12 mM K+ to the bath in the presence and absence of NE. Reactivation of the pump caused hyperpolarization of membrane PDs, and alpha(Nai) recovered monotonically in 3-5 min. The peak hyperpolarizations of V-1 and Vt (similar to 1 min) were significantly larger in the presence of NE. During the first 3 min, and also at the same alpha(Nai), the rate of decrease of alpha(Nai) was significantly faster in the presence of NE. In conclusion, these results show a direct effect of NE on cell membrane PDs and alpha(Nai) in the kidney proximal tubule. Most likely, beta-receptors are involved in mediating the action of NE. Neither Na/H exchange nor Na-substrate cotransport at the luminal membrane are affected by NE. On the other hand, NE activates Na-K-ATPase.