Electrical events in cardiac adrenergic nerves and noradrenaline release from the heart induced by acetylcholine and KCl

The effects of cholinomimetic drugs on responses to sympathetic nerve stimulation and noradrenaline in the rabbit ear artery

“…The facilitatory effect of acetylcholine on responses to nerve stimulation could be due to excitation of sympathetic terminal axons, as has been demonstrated in the cat spleen (Ferry, 1963) and the perfused cat heart (Cabrera, Torrance & Viveros, 1966;Haeusler et al, 1968). Acetylcholine sets up antidromic action potentials in the sympathetic nerves of these organs.…”

“…Since methacholine is virtually devoid of nicotinic activity, and muscarine reduced the responses to sympathetic nerve stimulation, it is suggested that impairment of noradrenaline release may result from an action of cholinomimetic drugs on muscarinic receptors of terminal adrenergic neurones. Other evidence for such receptors has been advanced by Lindmar et al (1968), who found that acetylcholine reduced the amount of noradrenaline released by dimethylphenylpiperazinium from the isolated perfused rabbit heart, and by Haeusler et al (1968), who observed that atropine increased about 80-fold the amount of noradrenaline liberated from the isolated perfused cat heart by acetylcholine.…”

“…Acetylcholine sets up antidromic action potentials in the sympathetic nerves of these organs. Haeusler et al (1968) showed that atropine reduced the antidromic excitation caused by acetylcholine although it increased the output of noradrenaline from the perfused cat heart, an observation which indicates that noradrenaline release by acetylcholine may be independent of the production of action potentials. Furthermore, they found that the muscarinic drugs, pilocarpine and methacholine, did not cause antidromic excitation.…”

“…Since nicotine acted like acetylcholine in the experiments cited, and since the actions of acetylcholine were exhibited in the presence of atropine, these excitatory and inhibitory effects of acetylcholine were taken to be nicotinic. However, a muscarinic action of acetylcholine on noradrenergic axons has been demonstrated by Lindmar, Loffelholz & Muscholl (1968) and by Haeusler, Thoenen, Haefely & Huerlimann (1968). They showed, first, that acetylcholine, methacholine and pilocarpine caused a reduction in the amount of noradrenaline released from the perfused rabbit or cat heart by nicotine and dimethylphenylpiperazinium, and, second, that the inhibitory effects of these drugs on noradrenaline release were abolished by atropine.…”

Parasympathetic excitation of sympathetic innervation after cholinesterase inhibition

“…Sympathetic nerve terminals possess both inhibitory muscarinic and excitatory nicotinic receptors on their axonal membranes (Haeusler et al, 1968;Stjarne, 1975;Westfall, 1977;1980;Starke, 1981;Levy, 1990;Todorov et al, 1991). While the muscarinic receptors apparently have a higher affinity for acetylcholine (Haeusler et al, 1968), evidence has been provided to suggest that full activation of the nicotinic receptors has more powerful effects on the nerve terminal membrane than does activation of the muscarinic receptor population (Westfall & Hunter, 1974). In rat periorbital smooth muscle, the action of parasympathetically released ACh is believed to be restricted under normal conditions to the inhibitory muscarinic receptors (Beauregard & Smith, 1994), thus the inhibitory action of parasympathetic stimulation on sympathetic neurotransmission.…”