Norepinephrine stimulation of sodium transport in Necturus urinary bladder

Abstract

Norepinephrine alters the transepithelial electrical properties of an open-circulated urinary bladder from the mud puppy, Necturus maculosus. When 10 −5 M norepinephrine is superfused over the serosa of the epithelium, the transepithelial voltage ( V t ) and short-circuit current ( I sc increase s the ( R t decreases. The norepinephrine-mediated changes are reversed by the addition of amiloride (5 · 10 −5 M) to the mucosal Ringer's solution. The serosal adrenoceptors mediating the Na + transport are more sensitive to norepinephrine ( EC 50 = 1.2 · 10 −6 M ) than to epinephrine or isoproterenol. Since the I sc is blocked selectively by the antagonist, phenoxybenzamine, stimulation of active transepithelial Na +-flux by catecholamines is mediated by an α-adrenoceptor. The apical cell membrane voltage ( V a ) and fractional resistance ( fR a ) were recorded using conventional KCl-filled microelectrodes. Untreated tissues have V a close to 0 mV while the basolateral membrane voltage ( V b ) is between −85 and −95 mV. About 90% of R t is apical cell membrane resistance ( fR a ). When amiloride inhibits sodium transport, V a becomes negative, V b hyperpolarizes slightly and fR a increases to 97%. On the other hand, if the bladders are treated with norepinephrine, fR a decreases to 79% as V a becomes positive and V b depolarizes. When R t changes, the resistance of the paracellular pathway ( R p ) is unaltered. Changes in the electrical properties of the tissue appear to be mediated primarily by alterations in R a . Since the Necturusbladder does not respond to antidiuretic hormone, this study implies that biogenic amines regulate Na + transport in the epithelium.