Electrophysiological analysis of beta-receptor stimulation in salamander proximal tubules

Electrophysiological response to isoproterenol stimulation was studied in isolated perfused salamander proximal tubules. The addition of 10(-5) M isoproterenol to the bath superfusate depolarized both the cell membrane, and transepithelial potentials by 2.2 +/- 0.2 and 0.31 +/- 0.04 mV, respectively (P less than 0.01, n = 35) and significantly reduced the apical-to-basolateral membrane resistance ratio by 30% (P less than 0.01, n = 7) from a control value of 3.7 +/- 0.6. These responses were blocked by 10(-6) M propranolol but not mimicked by 10(-4) M adenosine 3',5'-cyclic monophosphate. Qualitatively similar effects were observed with 10(-3) and 10(-7) M isoproterenol. Further characterization of the 10(-5) M isoproterenol response revealed 1) a 50% reduction in the response following the removal of organic substrates from the luminal perfusate, 2) an absolute requirement for sodium, and 3) an absolute requirement for a functioning basolateral Na+-K+-ATPase. The data suggest that beta-receptor stimulation may increase sodium reabsorption by activating sodium cotransport systems.