Electrical responses of cultured porcine thyroid cells to adrenergic agents.

Abstract

The membrane potential of cultured porcine thyroid follicular cells depolarized by up to 20 mV from the resting value of about -73 mV on exposure to beta-adrenoceptor agonists. A similar response was induced by TSH or dibutyryl cyclic AMP. alpha-Adrenoceptor agonists were without effect. The receptor subtype was shown to be (at least predominantly) beta 2 by the order of potency for beta-agonists (isoprenaline approximately equal to fenoterol much greater than adrenaline greater than noradrenaline) and by the relative potency of selective beta-antagonists (ICI 118,551 much greater than atenolol). The alpha-agonist phenylephrine had no effect on the TSH response but weakly inhibited the beta-agonist response. Rather than a physiological antagonism between alpha- and beta-adrenoceptor-mediated responses, this effect was shown to be due to the weak beta-antagonist effect of phenylephrine since the alpha-antagonist phentolamine failed to potentiate the depolarizing response to the mixed agonist noradrenaline, and also failed to block the inhibitory action of phenylephrine on the beta-agonist effect. Sensitivity to beta-agonist was enhanced by omission of serum from the culture medium and reduced by exposure to beta-agonists or a high concentration of TSH or dibutyryl cyclic AMP.