Nicotine peripheral nervous system effects

Diazinon, an anticholinesterase organophosphate, inhibits acetylcholinesterase in the central and peripheral nervous system. Inhibition of acetylcholinesterase results in accumulation of acetylcholine at muscarinic and nicotinic receptors leading to peripheral and central nervous system effects. These effects... 

Nicotine is known to bind to acetylcholine receptors (the receiving areas on cells) that are located throughout the central nervous system as well as the peripheral nervous system. Acetylcholine is a neurotransmitter it transmits nerve impulses from one nerve fiber to another. The pleasurable effects of nicotine are a... 

Mecfianism of Action A cholinergic-receptor agonist that binds to acetylcholine receptors, producing both stimulating and depressant effects on the peripheral and central nervous systems. Therapeutic Effect Provides a source of nicotine during nicotine withdrawal and reduces withdrawal symptoms. 

Bethanechol Muscarinic agonist t negligible effect at nicotinic receptors Activates Mi through M3 receptors in all peripheral tissues causes increased secretion, smooth muscle contraction (except vascular smooth muscle relaxes), and changes in heart rate Postoperative and neurogenic ileus and urinary retention Oral and parenteral, duration 30 min does not enter central nervous system (CNS) Toxicity Excessive parasympathomimetic effects, especially bronchospasm in asthmatics Interactions Additive with other parasympathomimetics... 

Lockett (36, 37) has described two compounds, base A and base B. Base A occurred in the urine of men (who smoked), women (who did not smoke), and bitches. There was approximately three times as much in the urine of men and bitches as of women. The base was somewhat more active pharmacologically than Z-nicotine, and was found to exert its pressor effect through the mediation of the corpus striatum and thalamus, stimulating the sympathetic nervous system (38). Base A could be converted to -nicotine by drying in a high vacuum, with alteration of its action from a central to a peripheral one therefore it must be very similar in structure to nicotine. Base B was a different compound, also with pressor activity both were obtained by steam distillation from strongly alkaline urine. Furthermore, another compound, which she called base x, appeared in the... 

As with the mental effects of nicotine, the physiological effects are brought about by its actions on the nervous system, both peripheral and central. Nicotine changes the transmission of nerve impulses by binding to acetylcholine receptors, and induces the release of several chemical messengers, which in turn affect several body systems. 

In the peripheral (Wessler 1989) as well as central (Wonnacott 1997) nervous system, presynaptic nicotinic autoreceptors were reported to control the release of acetylcholine. In both locations, the consequence of presynaptic nAChR activation most commonly is an increase in both spontaneous and evoked acetylcholine release (MacDermott et al. 1999), whereas presynaptic muscarinic receptors mediate the opposite effect, an autoinhibition. Recent studies have focused on the composition of presynaptic nAChRs (Table 2). In the hippocampus, nicotinic autoreceptors were suggested to be a3/p4 receptors (Tani et al. 1998), but a role of p2 subunits has also been implicated (Lloyd et al. 1998). Likewise, in the neocortex, presynaptic nicotinic autoreceptors are likely to be 04/ p2 receptors (Marchi et al. 2002). In contrast, in the interpeduncular nucleus the autoreceptors were suggested to mainly contain a3 and p4 subunits (Grady et al. 2001). 

Q2 Both the central and peripheral parts of the nervous systems have been affected by the insecticide, which has produced effects mediated by both muscarinic and nicotinic receptors. 

The greatest hazard to life arises from suppression of the ability to secrete sweat, which can give rise to fatal hyperthermia if body temperature is not controlled artificially during hot weather or strenuous activity. Another source of hazard to life arises from the effect of the compounds other than scopolamine and its quaternary form in accelerating heart rate and facilitating Intramural conduction and transmission of Impulses. Ihese actions may result in serious arrhythmias up to and including ventricular fibrillation. The quaternary amine forms of the tropic acid esters in which we are interested are more active in some respects than the tertiary amines, as far as peripheral actions are concerned. This is especially true with respect to actions on nicotinic effectors in ganglia and striated muscles. The quaternary amines penetrate into the central nervous system poorly, but, once there, affect muscarinic effectors in the same way as the tertiary amines. 

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