Presence of muscarinic inhibitory and absence of nicotinic excitatory receptors at the terminal sympathetic nerves of chicken hearts

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Abstract
Nicotine (2×10−4 M) or acetylcholine (5.5×10−4 M) in the presence of 3×10−6 M atropine did not increase the rate or amplitude of contraction in isolated atria or ventricular strips of the chicken heart; both drugs also did not cause an output of noradrenaline or adrenaline and did not evoke antidromic discharges in the right sympathetic nerves of isolated perfused chicken hearts. In contrast, “high K+-solutions” evoked an output of noradrenaline and adrenaline and caused a burst of antidromic discharges. Dimethylphenylpiperazine (DMPP; 3.1×10−4 M), by a tyramine-like action, elicited a small output of noradrenaline and increased rate and amplitude of contraction, but did not evoke antidromic discharges. The noradrenaline output caused by DMPP was not reduced by lowering the extracellular Ca2+ concentration from 1.8 to 0.1125 mM.-Acetylcholine (10−5 and 10−4 M) inhibited the noradrenaline and adrenaline outputs evoked by electrical stimulation of the right sympathetic nerves (3 Hz, 1 ms, 30 V); the inhibition was blocked by 3×10−6 M atropine. —It is concluded that the terminal parts of sympathetic nerves of the chicken heart posses muscarinic inhibitory receptors but lack nicotinic excitatory receptors. Thus prejunctional nicotinic receptors are not an integral part of the terminal sympathetic neurone otherwise they would be present at this neurone in all species.

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