Pharmacodynamics nicotine

Clark MS, Rand Ml, Vanov S (1965) Comparison of pharmacological activity of nicotine and related alkaloids occurring in cigarette smoke. Arch Int de Pharmacodynamic et de Therapie 156 363-379... 

Rosecrans JA, Chance WT (1978) The discriminative stimulus properties of n- and m-cholinergic receptor stimulants. In Ho BT, Richards DW III, Chute DL (eds) Drug discrimination and state dependent learning. Academic, New York, pp 119-130 Rosecrans JA, Schechter MD (1972) Brain area nicotine levels in male and female rats of two strains. Arch Int de Pharmacodynamic et de Therapie 196 46-54 Rosecrans JA, Kallman MJ, Glennon RA (1978) The nicotine cue an overview. In Colpaert EC, Rosecrans JA (eds) Stimulus properties of drugs ten years of progress. Elsevier-North Holland, Amsterdam, pp 69-81... 

Henningfield JE, Miyasato K, Jasinski DR (1985) Abuse hability and pharmacodynamic characteristics of intravenous and inhaled nicotine. J Pharmacol Exp Ther 234 1-12... 

Byrd GD, Davis RA, Caldwell WS, Robinson JH, deBethizy JD (1998) A further study of FTC yield and nicotine absorption in smokers. Psychopharmacology 139 291-299 Chaudhri N, Caggiula AR, Donny EC, Palmatier MI, Liu X, Sved AF (2006) Complex interactions between nicotine and nonpharmacological stimuli reveal multiple roles for nicotine in reinforcement. Psychopharmacology 184 353-366 Cone EJ (1995) Pharmacokinetics and pharmacodynamics of cocaine, J Analy Toxicol 19 459 78 Desai RI, Terry P (2003) Evidence of cross-tolerance between behavioural effects of nicotine and cocaine in mice. Psychopharmacology 166 111-119 Desai RI, Barber DJ, Terry P (1999) Asymmetric generalization between the discriminative stimulus effects of nicotine and cocaine, Behav Pharmacol 10 647-656... 

Pickworth WB, Fant RV, Nelson RA, Rohrer MS, Henningfield JE (1999) Pharmacodynamic effects of new de-nicotinized cigarettes. Nicotine Tob Res 1 357-364 Piehl DH (1978) Nicotine and smoker satisfaction. 04 Jan 1978. R.J. Reynolds. Bates 504423322-504423327. http //tobaccodocuments.org/filters/504423322-3327.html Potter DL (1991) Project Wd. 1991. R.J. Reynolds. Bates 508114925-508114926. http // tobaccodocuments.org/product design/508114925 926.html Read G (1984) Nicotine conference details. 02 May 1984. Brown Williamson. Bates 512106427-512106437. http //tobaccodocuments.org/product esign/36816.html Reininghaus W (1987) [No title]. 02 Sep 1987. Philip Morris. Bates 2023186690. http // tobaccodocuments.org/pm/2023186690.html... 

Cone EJ (1995) Pharmacokinetics and pharmacodynamics of cocaine, J Anal Toxicol 19 459-78 Cryan JF, Bruijnzeel AW, Skjei KL, Markou A (2003) Bupropion enhances brain reward function and reverses the affective and somatic aspects of nicotine withdrawal in the rat. Psychopharmacology 168 347-358... 

Pant RV, Henningfield JE, Nelson RA, Pickworth WB (1999) Pharmacokinetics and pharmacodynamics of moist snuff in humans. Tob Control 8 387-392 Pant RV, Henningfleld JE, Shiffman S, Strahs KR, Reitberg DP (2000) A pharmacokinetic crossover study to compare the absorption characteristics of three transdermal nicotine patches. Pharmacol Biochem Behav 67 479 82... 

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. 

Influence of other medicinal products which are normally administered concomitantly. Possible pharmacodynamic and pharmacokinetic interactions with other medicinal products or substances like alcohol, caffeine, tobacco, nicotine. 

Pahner KJ, Bnckley MM, Fanlds D. Transdermal nicotine. A review of its pharmacodynamic and pharmacokinetic properties, and therapentic efficacy as an aid to smoking cessation. Drngs 1992 44(3) 498-529. 

Data shall be presented on the pharmacodynamic (pharmacokinetic) interactions of the medicinal product with other substances or medicinal products, including also alcohol, tobacco or nicotine in cases of intake. The data shall be described and discussed from the view point of their significance and connection with the drug interactions indicated in the summciry of product characteristics. 

This chapter considers individual differences in the pharmacology of nicotine. While there is evidence of genetic difference in pharmacologic response to nicotine in rodents (Marks et al. 1991), there has been very little research into individual differences in pharmacodynamics in humans. Individual differences in pharmacokinetics and metabolism have been much better documented, and are the major focus of this discussion. 

The pharmacodynamic action of the nicotine derivatives, such as the a- and a -aminonicotines and a- and a -acetylaminonicotine, was studied by Mednikian (80). The respiratory stimulation which these substances provoke is less pronounced than that produced by nicotine but is more durable. As for the acetylated derivatives, this action is not preceded by an initial respiratory arrest which many other substances in the nicotine group presented. These substances act on the chemoceptors of the carotid body, on the respiratory center itself, and on the intrapulmonary endings of the vagus. 

Mescaline, a constituent of some Mexican cacti, does not have any demonstrable stimulating effect on the respiration. However, according to Dixon (189), the injection of mescaline in the cat (25 mg./kg.) provokes a slowing and an increase in the respiratory depth followed by an increase in its rate. Repeated injections of this alkaloid cause the respiratory movements to become slower and slower. The pharmacodynamic action of mescaline is rather characteristic, but in certain points it resembles strychnine, nicotine, digitalin, and cocaine. 

Teeguarden JG, Housand CJ, Smith JN, Hinderliter PM, Gunawan R, Timchalk CA. A multi-route model of nicotine-cotinine pharmacokinetics, pharmacodynamics and brain nicotinic acetylcholine receptor binding in humans. Regal Toxicol Pharmacol 2013 65(l) 12-28. 

In pharmacodynamics, the parallel phenomenon to resistance is the loss of effect of a drug, either through the body having learnt to degrade it (as happens with barbiturates, Section 3.4) or by the sensitivity of the receptor apparently declining (as happens with nicotine and morphine). 

Because they are so reactive, even at small doses, most alkaloid-rich plants are used sparingly, if at all, in Western herbalism. Indeed, use of many of the alkaloidal species is restricted by law, or listed on poison schedules. However, alkaloids—either as isolated compounds or their semi-synthetic derivatives—are widely used in pharmaceutical medicines. Much of our understanding of the mechanisms of neurotransmitters and receptor sites comes from research into the pharmacodynamics of alkaloids. The widespread use of terms such as nicotinic and muscarinic receptors supports this idea. 

When designing a dmg to be a cholinergic agonist, selectivity is highly desirable but not a simple term, as therapeutic candidates should be selective for the cholinergic receptor among other neurological receptors, selective for nicotinic or muscarinic, or selective for spedfic subtypes or tissue types. Selectivity could be achieved on the pharmacodynamic level, where the stmcture of the dmg molecule makes it more active at one receptor than another, or on the pharmacokinetic level where the molecular stmcture of the dmg makes it more available to spedfic tissues. Equally important, the new stmcture should retain ACh s activity (see Box 16.1). 

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