HYPERPOLARIZING ‘α2’‐ADRENOCEPTORS IN RAT SYMPATHETIC GANGLIA

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Abstract
1 Receptors mediating catecholamine-induced hyperpolarization of isolated superior cervical sympathetic ganglia of the rat have been characterized by means of an extracellular recording method. 2 (—)-Noradrenaline (EC50, 1.7 ± 0.6 μm) produced an immediate low-amplitude (2+ or on reduction of external K+ from 6 to 2 mm. Hyperpolarization was unaffected by changing the temperature from 25° to 37°C. 3 Hyperpolarization was also produced by the following agonists (potencies relative to (—)-noradrenaline): (—)-noradrenaline 1; (±)-isoprenaline 0.41; (—)-phenylephrine 0.40; (+)-noradrenaline 0.13; 2-amino-6,7-dihydroxy tetrahydronaphthalene (ADTN) 0.25; dopamine 0.1; methoxamine 0.012; amidephrine 0.0015. 4 Responses were antagonized by phentolamine (1 μm) but not by (±)-propranolol (1 μm), haloperidol (10 μm) or α-flupenthixol (1 μm). This suggested that hyperpolarization was mediated solely throughα-receptor stimulation not through stimulation of β-receptors or dopamine-receptors. 5 Dose-ratio shifts produced by phentolamine varied with different agonists. The shift increased in inverse proportion to the ability of the agonists to inhibit [3H]-(—)-noradrenaline uptake, suggesting that uptake of agonists limited the dose-ratio shift. Cocaine and nortriptyline reduced catecholamine-induced hyperpolarization in concentrations (10 μm and 1 μm respectively) necessary to inhibit [3H]-(—)-noradrenaline uptake. 6 Clonidine (0.01 to 1 μm), oxymetazoline (0.01 to 1 μm) and ergometrine (0.1 to 10 μm) produced a persistent, low-amplitude hyperpolarization, as though they were partial agonists. Responses to the agonists were blocked by yohimbine (1 μm) but not be prazosin (1 μm). 7 It is concluded that the adrenergic cell bodies in the ganglion were hyperpolarized through activation of the same type ofα-receptor (‘α2-receptors’) as those present at adrenergic nerve terminals.