AJP - Renal Physiology, Vol 261, Issue 3 393-F399, Copyright © 1991 by American Physiological Society
Evidence for presence of functional beta-adrenoceptor in rabbit S2 proximal straight tubules
K. Kudo, Y. Kondo, K. Abe, Y. Igarashi, K. Tada and K. Yoshinaga
Department of Clinical Biology and Hormonal Regulation, Tohoku University School of Medicine, Sendai, Japan.
The effect of isoproterenol on the electrophysiological properties of the
S2 proximal segment of the rabbit was examined. Isoproterenol at 10(-8) to
10(-4) M depolarized the basolateral membrane voltage (Vb) in a
dose-dependent manner. Propranolol attenuated the isoproterenol-induced
depolarization. These possible mechanisms of cell depolarization were
explored. The role of luminal Na(+)-organic solute cotransport was
negligible, since the removal of organic solute did not change the
depolarization. Basolateral Na(+)-(HCO3-) cotransport was supported by the
finding that 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid inhibited
isoproterenol-induced depolarization. Basolateral K+ conductance was
suggested by the finding that the application of Ba2+ blocked the
isoproterenol-induced depolarization. Na(+)-K(+)-adenosine-triphosphatase
(ATPase) was questionable. Although ouabain blocked isoproterenol-induced
depolarization, the removal of Na+ did not inhibit the depolarization.
Further experiment revealed that dibutylyl-adenosine 3',5'-cyclic
monophosphate (cAMP), 8-bromo cAMP, and forskolin did not mimic the
response of isoproterenol. These results demonstrate: 1) there is a
functional beta-adrenoceptor that depolarizes Vb; 2) isoproterenol-induced
depolarization is due to an inhibition of basolateral K+ channel or the
activation of basolateral Na(+)-(HCO3-)n cotransport; 3)
isoproteronol-induced depolarization is independent of cAMP in the rabbit
proximal tubule.
