Nicotine autonomic effects

Acetylcholine antagonists (blockers) that block the nicotine-like effects (neuromuscular blockers and autonomic ganglion blockers) are described elsewhere (see Ch. 18). 

Adverse reactions to treatment with diethylcarbamazine vary with the infecting filarial species and are most severe in onchocerciasis. Minor reactions include malaise, nausea, and headache, but diethylcarbamazine also depresses the central nervous system in some individuals, resulting in dizziness and somnolence reversible coma has been reported in patients in poor physical condition. Nicotine-like properties can produce autonomic effects. A degree of eosinophilia during treatment is usual. 

Another point to notice in Table 7.5 is nicotine s autonomic effects, particularly on the cardiovascular system. The stimulation of the heart and its resultant increased demands for oxygen underlie the association of nicotine and heart disease. In this regard, a less than adequate supply of oxygen to the heart may result in chest pain (angina) or a heart attack (Julien, 2005). 

Nicotinic Autonomic ganglia Sympathetic effects, including pallor, tachycardia, hypertension... 

Drugs that block the nicotinic receptors on autonomic ganglia, such as hexamethonium, probably do so by actually blocking the Na+ ion channel rather than the receptor. Generally these receptors appear to resemble the central ones more than those at the neuromuscular junction and dihydro-jS-erythroidine is one drug that it is an effective antagonist in both ganglia and the CNS. 

Nicotine is an addictive substance with rewarding and reinforcing properties. On the other hand, the autonomic responses following an acute nicotine treatment and the bitter taste of nicotine may cause aversion. This aversion may impact conditioned effects to nicotme. Rinker et al. (2008) studied possible sex differences in taste aversion mduced by nicotine in rats systemic nicotine or saline injections were paired wim oral saccharine. Although nicotme did produce a weak taste aversion, no sex differences were observed, excluding the possible contribution of the aversive properties of nicotine on sexually dimorphic responses to nicotine. The authors conclude that sex differences may arise from differences in the rewardmg properties of the drug. 

Atropine, an alkaloid from Atropa belladonna, is the classical parasympatholytic compound. It competes with acetylcholine for the binding at the muscarinic receptor. Its affinity towards nicotinic receptors is very low, so that it does not interfere with the ganglionic transmission or the neuromotor transmission, at least in therapeutic dosages. However, in the central nervous system muscarinic receptor do play an important role and while atropine can penetrate the blood-brain barrier it exerts pronounced central effects. Atropine, like all other antagonists of the muscarinic acetylcholine receptor inhibit the stimulatory influence of the parasympathetic branch of the autonomous nervous system. All excretory glands (tear, sweat, salivary, gasto-intestinal, bronchi) are... 

The administration of acetylcholine mimics the stimulatory effect of nicotine, the alkaloid from the tobacco plant, on autonomic ganglia and the adrenal medulla. It has become common practice to refer to the effects of acetylcholine on visceral effectors as the muscarinic action of acetylcholine and to its effects on the... 

Nicotine is a tertiary amine compound composed of a pyridine and a pyrrolidine ring. It binds selectively to acetylcholine receptors at the autonomic ganglia in the adrenal medulla at neuro-muscular junction and in the brain. It exerts a stimulating effect in the cortex and a reward effect via the pleasure system in the limbic system. 

Most of the direct organ system effects of muscarinic cholinoceptor stimulants are readily predicted from a knowledge of the effects of parasympathetic nerve stimulation (see Table 6-3) and the distribution of muscarinic receptors. Effects of a typical agent such as acetylcholine are listed in Table 7-3. The effects of nicotinic agonists are similarly predictable from a knowledge of the physiology of the autonomic ganglia and skeletal muscle motor end plate. 

The actions of acetylcholine released from autonomic and somatic motor nerves are terminated by enzymatic hydrolysis of the molecule. Hydrolysis is accomplished by the action of acetylcholinesterase, which is present in high concentrations in cholinergic synapses. The indirect-acting cholinomimetics have their primary effect at the active site of this enzyme, although some also have direct actions at nicotinic receptors. The chief differences between members of the group are chemical and pharmacokinetic—their pharmacodynamic properties are almost identical. 

Acetylcholine receptors are classified as either muscarinic cholinergic receptors or nicotinic cholinergic receptors. The alkaloid muscarine mimics the effects produced by stimulation of the parasympathetic system. These effects are postganglionic and are exerted on exocrine glands, cardiac muscle, and smooth muscle. The alkaloid nicotine mimics the actions of acetylcholine, which include stimulation of all autonomic ganglia, stimulation of the adrenal medulla, and contraction of skeletal muscle. 

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