Prolonged exposure to β‐adrenergic agonists of pigeon erythrocytes causes a reversible loss (70%) of catecholamine‐stimulated adenylate cyclase activity without reduction in the number of β‐adrenergic receptors. In addition a less pronounced decrease in non‐stimulated and NaF‐stimulated adenylate cyclase activity (15–22%) is observed, appearing at different agonist concentrations and at a different rate. Dibutyryladenosine 3′,5′‐phosphate and the phosphodiesterase inhibitor methylisobutylxanthine partially mimick the action of the β ‐adrenergic agonist, thus pointing to a possible role of adenosine 3′,5′‐phosphate in establishing desensitization. When adenylate cyclase from desensitized cells is stimulated with 5′‐guanylyl‐imidodiphosphate in the presence or absence of catecholamines the lag period preceding the attainment of maximal activity is extended. Likewise the rate of reversal by GTP or ATP of persistent activation of adenylate cyclase is slowed down. This is therefore interpreted to mean that the loss in hormonal ‐stimulation on treatment of pigeon red blood cells with β‐adrenergic agonists is due to a delayed exchange of GDP against GTP on the regulatory GTP‐binding protein. Furthermore, we conclude that events causing the refractory state in avian erythrocytes should occur at a site distal to the β‐adrenergic receptor.
|Original language||English (US)|
|Number of pages||6|
|Journal||European Journal of Biochemistry|
|State||Published - Oct 1980|
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