Journal of Neurophysiology, Vol 68, Issue 1 117-123, Copyright © 1992 by APS
Isoproterenol enhances a calcium-independent potassium current in mouse anterior pituitary tumor cells
R. Weik and J. Spiess
Department of Molecular Neuroendocrinology, Max Planck Institute for Experimental Medicine, Goettingen, Federal Republic of Germany.
1. The patch-clamp technique was used to study the action of the
beta-adrenergic agonist (-)-isoproterenol in anterior pituitary tumor cells
of the mouse. 2. (-)-Isoproterenol induced an inward-rectifying potassium
conductance with half-maximal stimulation at a concentration of
approximately 67 nM. The isomer (+)-isoproterenol was less effective in
stimulating the current. 3. The effect of (-)-isoproterenol was abolished
by cholera toxin treatment, indicating the involvement of a Gs protein,
whereas pertussis toxin treatment did not exhibit a current reduction. 4.
We blocked or stimulated phosphorylation pathways in cells to test the
involvement of adenosine 3',5'-cyclic monophosphate (cAMP). It was
concluded that the current stimulation probably was not exclusively
mediated by cAMP. 5. Activation of calcium-dependent potassium channels by
an isoproterenol-induced calcium influx into the cell could be excluded. 6.
Therefore it is suggested that the observed activation of a potassium
current by isoproterenol could be directly mediated by a Gs protein.
