Relation between catecholamine‐induced cyclic AMP changes and hyperpolarization in isolated rat sympathetic ganglia

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Abstract
1. The effect of catecholamines on cyclic adenosine 3′5′‐monophosphate (cyclic AMP) production in isolated rat superior cervical ganglia has been measured under experimental conditions in which they also produce ganglion hyperpolarization. 2. (±)Isoprenaline (1 μ M) increased cyclic AMP levels by 8‐100 times after 15 min incubation at 25 °C. Half‐maximal stimulation occurred at about 0.03 μ M. This was due to stimulation of β‐receptors, since it was prevented by 1 μ M‐propranolol but not by 1 μ M‐phentolamine. 3. The α‐agonists phenylephrine (100 μ M), dopamine (100 μ M) and clonidine (1 μ M) did not produce a detectable increase in ganglionic cyclic AMP. Dopamine (100 μ M) was also ineffective at 37 °C in the presence of 10 m M‐theophylline. 4. Exogenous cyclic AMP (0.01‐1 m M) hyperpolarized the ganglion. This effect was replicated by other adenosine compounds, most effectively by adenosine and by adenosine 5′‐monophosphate, and was antagonized by theophylline. Dibutyryl cyclic AMP was weaker than cyclic AMP. 5. Neither theophylline nor the non‐xanthine phosphodiesterase inhibitor, Ro 20‐1724, enhanced the hyperpolarizing actions of noradrenaline or dopamine. 6. Since catecholamine‐induced hyperpolarization of the isolated rat ganglion is induced via α‐receptors, whereas cyclic AMP‐production is induced via β‐receptors, it is concluded that cyclic AMP is unlikely to mediate the hyperpolarization. The effect of exogenous cyclic AMP may be due to an action on external adenosine‐receptors.