Letter | Published:

Chronic guanethidine treatment increases cardiac β-adrenergic receptors

Abstract

VARIOUS pharmacologically active agonists capable of altering cell function have been shown to interact primarily with specific receptors on the outer cell membrane1. Evidence has accumulated from several systems to suggest that there may be a dynamic and inverse relationship between the number or density of receptors on the membrane surface and the degree of receptor occupancy by agonist2,3. We present here experiments which demonstrate in rat hearts that chronic withdrawal of adrenergic stimulation produced by guanethidine treatment in vivo results in increased cardiac β-adrenergic receptor density. Further, in isolated, perfused hearts obtained from guanethidine-treated animals, there is an increased cyclic AMP (cAMP) accumulation in response to the β-adrenergic agonist isoprenaline, suggesting that the increased numbers of receptors may be related to the increased biochemical response.

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