Electrophysiological studies in principal cells of rat cortical collecting tubules. ADH increases the apical membrane Na+-conductance.

The mechanism of ion transport across principal cells of rat cortical collecting tubules (CCT) and its regulation by vasopressin (ADH) has been studied in the isolated perfused tubule. To amplify the response to ADH rats were treated with 5 mg I. M. desoxycorticosterone 4-9 days prior to the experiments. Addition of 2 X 10(-10) mol X l-1 ADH increased the transepithelial voltage from -5.1 +/- 0.7 mV to -16.1 +/- 1.4 mV (n = 37) and decreased the transepithelial resistance from 51 +/- 4 omega cm2 to 39 +/- 2 omega cm2 (n = 33). Optical and functional differentiation of impalements of principal and intercalated cells was made and only data of principal cells are presented. ADH depolarized the apical membrane from 79 +/- 1 mV to 66 +/- 2 mV (n = 26) and decreased the fractional resistance of the apical membrane from 0.76 +/- 0.04 to 0.70 +/- 0.04 (n = 13). These ADH effects were prevented by 10(-5) or 10(-4) mol X l-1 luminal amiloride which hyperpolarized the apical membrane when added in the presence or absence of ADH. Apical and basolateral membranes were dominated by large K+ conductances and addition of 3 mmol X l-1 barium to bath or lumen perfusates increased transepithelial resistance almost two-fold, whereas luminal amiloride increased the transepithelial resistance only by 26-35%. Ouabain (0.5 mmol X l-1, bath) depolarized the basolateral membrane and decreased its K+ conductance. These effects were prevented by the simultaneous presence of apical amiloride suggesting that the only route of Na+ entry into the principal cells occurred via the amiloride sensitive Na+ conductance. We conclude that ADH stimulates Na+ reabsorption and K+ secretion in the rat CCT primarily by increasing the Na+ conductance in the apical cell membrane.