EFFECTS OF SYMPATHETIC INNERVATION AND TEMPERATURE ON THE PROPERTIES OF RAT HEART ADRENOCEPTORS

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Abstract
1 The pharmacological characteristics of adrenoceptors at different temperatures were assessed on the basis of the effects of various α- and β-adrenoceptor agonists and antagonists on electrically-driven left atria and spontaneously-beating pairs of atria from rats. 2 Phenoxybenzamine (Pbz) potentiated inotropic responses of left atria to noradrenaline (NA) at 31°C, produced significantly less potentiation at 24°C and inhibited responses at 17°C; it had little effect on responses to CaCl2. Both Pbz and phentolamine inhibited responses to phenylephrine more effectively at 17 than at 31°C. N-cyclohexylmethyl-N-ethyl-β-chloroethylamine hydrochloride (GD-131), a haloalkylamine with negligible α-adrenoceptor blocking activity, caused only potentiation of responses to NA at 17°C. 3 The presence of phentolamine during incubation with Pbz eliminated block of responses to NA and revealed a potentiation that was equivalent at all three temperatures tested. Phentolamine did not alter the block of responses to 5-hydroxytryptamine by Pbz. Protection of α-adrenoceptors by phentolamine during exposure to [3H]-Pbz significantly decreased the amount of label bound to the myocardium at 17°C, but did not alter binding at 31°C. 4 Inhibition of responses to NA by propranolol decreased with temperature, and the magnitude of the change increased with the concentration of propranolol. Compared to 31°C, the effect of the highest concentration of propranolol. (4.0 μM) was significantly decreased at 24°C, and the effects of all except the lowest concentration (0.04 μM) were significantly decreased at 17°C. 5 The potency of isoprenaline decreased and that of phenylephrine increased at low temperatures, and their potency ratio was much lower at 17 than at 31°C for both the inotropic and chronotropic responses of spontaneously-beating atria. However, the ratio was unaffected by temperature in electrically-driven left atria. A similar difference between spontaneously-beating and driven preparations is apparent in the data of other workers, but its basis is not clear. 6 Atria from rats pretreated with 6-hydroxydopamine (6-OHDA) were sensitized to the effects of NA, and there was no increase in α-adrenoceptor properties at low temperatures. Little α-adrenoceptor activity could be demonstrated in chemically denervated atria at any temperature. 6-OHDA pretreatment did not alter the binding of [3H]-Pbz at 31°C, but decreased it significantly at 17°C. Pretreatment with reserpine caused some sensitization, but did not significantly alter the characteristics of the adrenoceptors or their responses to temperature. 7 It is concluded that the adrenoceptors of rat atria are affected by temperature in much the same way as those of frog hearts, although the transition from β- to α-adrenoceptor properties may begin at a slightly higher temperature. α-Adrenoceptor properties appear to require the presence of intact adrenergic nerves but not the presence of normal stores of neurotransmitter.