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At least 19 recordsLinked to original sources
PubMed1979

Optically pure (+)-nicotine from (+/-)-nicotine and biological comparisons with (-)-nicotine.

Optically pure (+)-nicotine has been obtained from (+/-)-nicotine using a combination of d-tartaric acid and di-p-toluoyl-l-tartaric acid. As the di-d-tartrate salt, (+)-nicotine is less potent than (-)-nicotine di-l-tartrate in producing lethality in mice, on blood pressure in anesthetized rats, and in the isolated guinea-pig ileum, indicating substantial stereospecificity for nicotine receptors. Potency ratios are 0.14, 0.06, and 0.019, respectively.

Animals↗
PubMed1979

Relations between nicotine-induced convulsive behavior and blood and brain levels of nicotine as a function of sex and age in two inbred strains of mice.

Nicotine levels in blood and whole brain were measured as a function of sex and age in C57BL/6J and DBA/2J mice and compared to the behavioral responses following an intraperitoneal injection of nicotine. The results indicate that blood levels of nicotine alone do not accurately predict either brain levels of nicotine or the behavioral responses to a single injection of nicotine. In general, brain levels of nicotine proved to be a fairly accurate predictor of the behavioral responses to nicotine. The data indicate that the sexes differ in their sensitivity to nicotine. Forty-two-day-old male mice of both strains given comparable doses of nicotine were found to concentrate the drug in the brain more than females. However, there was no corresponding increase in sensitivity to this increased brain concentration as measured by LD50, ED50, latency to tremor or latency to death.

Aging↗
PubMed1977

Development of nicotinic responses in the rat adrenal medulla and long-term effects of neonatal nicotine administration.

1. The development of nicotinic responses in the rat adrenal medulla was examined at various ages from 1 to 50 days of age by testing the ability of nicotine (10 mg/kg, s.c.) to deplete catecholamines and induce tyrosine hydroxylase. 2. Catecholamines were depleted 25% 3 h after injection of nicotine at all ages tested, but the degree of tyrosine hydroxylase induction 24 h after nicotine increased with age. 3. These data indicate that functional nicotinic receptors are present in the neonatal adrenal medulla before the development of functional splanchnic innervation, but that the development of the ability to induce tyrosine hydroxylase is not coupled directly to the development of secretory mechanisms. 4. The long-term effects of a single dose of nicotine (10 mg/kg, s.c.) administered to one day old rats were also examined. 5. After the short-term catecholamine depletion caused by nicotine, there were persistent elevations of catecholamines and tyrosine hydroxylase until 23 days of age; however, dopamine beta-hydroxylase remained elevated into young adulthood. 6. These data indicate that neonatal nicotine administration can produce long-term changes in adrenal catecholamine biosynthetic enzymes.

Adrenal Medulla↗
PubMedDate not supplied

Localization of nicotine-14C, cotinine-14C, and nicotine-1'-N-oxide-14C in tissues of the mouse.

The distrubutions of nicotine-14C (2'- or methyl-labeled), cotinine-14C, and nicotine-1'-N-oxide-14C were studied by whole-body autoradiography in mice and in perfused rabbit lung. The compounds were administered either iv, sc, ip, or by inhalation. Blank sections were also incubated with nicotine-14C and cotinine-14C in vitro. The distributions were compared in a black (C57BL/6J), brown (C57L/J), and albino (A/HeJ) strain and in CD-1 germ-free mice. After administration of nicotine-14C in vivo, radioactivity was localized in all strains in bronchi, nasal mucosa, salivary gland, Harder's gland, liver, kidney, stomach, spleen, pancreas, intestine, bone, gallbladder, and adrenal medulla. In the pigmented strains, it was also localized in melanin in the eye, brain, and hair. Radioactivity did not accumulate in the bronchi of late-term fetuses or the 1-day-old newborn but was present in the 2-day-old and older. Cotinine-14C and nicotine-1'-N-oxide-14C, after iv administration, did not localize in bronchi or nasal mucosa at short time intervals after injection. Frozen sections incubated in vitro did not accumulate either nicotine-14C or cotinine-14C in the bronchi; whereas the affinity for melanin was unchanged. Incubation of fresh, nonfrozen mouse lung and perfusion of rabbit lung in vitro with nicotine-14C produced the same localization of radioactivity in bronchi as that seen after in vivo administration. Preheating the frozen sections or lungs in a microwave oven before incubation did not change the localization of radioactivity in the bronchi or other tissues. The localization of radioactivity in bronchi may be due to metabolism, active transport, or binding of nicotine; this mechanism is destroyed by freezing the tissue.

Animals↗
PubMed1976

[Metabolism of nicotinic acid in plant cell suspension cultures, IV: Occurrence and metabolism of nicotinic acid N-alpha-arabinoside (author's transl)].

Application of nicotinic acid to cell suspension cultures of Petroselinum hortense Hoffm., Daucus carota, Nicotiana tabacum and Nicotiana glauca leads to the formation of the recently isolated[2] nicotinic acid N-alpha-L-arabinoside. In these cell cultures the arabinoside is a metabolically active compound; the nicotinic acid moiety is used for NAD synthesis and nicotinic acid degradation involving decarboxylation and ring fission. N-Methylnicotinic acid (trigonelline) and nicotinic acid N-alpha-L-arabinoside occur alternatively in plant cell suspension cultures, but seem to fulfil the same function as a reserve form for nicotinic acid. Catabolism of nicotinic acid in parsley cell suspension cultures does not involve 6-hydroxynicotinic acid as an intermediate.

Arabinose↗
PubMed1976

[Metabolism of nicotinic acid in plant cell suspension cultures: II; Isolation, characterization and enzymology of nicotinic acid N-alpha-arabinoside (author's transl)].

A very hydrophilic compound was isolated from parsley cell suspension cultures in high yield after application of nicotinic acid. Using chemical, chromatographic and spectroscopic procedures the structure of this new plant constituent has been elucidated as nicotinic acid N-alpha-L-arabinopyranoside. This structure has been proved by chemical synthesis. An arabinosyltransferase was isolated from parsley cell suspension cultures and purified about 19-fold. The enzyme converted nicotinic acid N-alpha-arabinoside with UDP to nicotinic acid and UDP-arabinose. pH-Optimum (pH 7.0-8.0), Km value for nicotinic acid N-alpha-L-arabinoside (2.2 X 10(-4) mol/l) and mol. wt. (app. 70 000) of the transferase were measured. Function and biosynthesis of the arabinoside in cell cultures are discussed.

Arabinose↗
PubMed1979

N-demethylation of nicotine and reduction of nicotine-1'-N-oxide by Microsporum gypseum.

Several microorganisms were examined for their abilities to convert S-nicotine into nornicotine. Five microorganisms including Microsporum gypseum (ATCC 11395) produced nornicotine and three unknown metabolites. M. gypseum efficiently reduced nicotine-1'-N-oxide to nicotine, but no nornicotine was obtained when the N-oxide was used as substrate.

Chemical Phenomena↗
PubMed1977

The mechanism of action of nicotine on vascular adrenergic neuroeffector transmission.

The aim of this study was to determine the site and mechanism of action of nicotine on sympathetic neuroeffector transmission in the isolated pulmonary artery of the rabbit. Nicotine and cocaine potentiated the constrictor response elicited by electrical-field stimulation of postganglionic adrenergic neurones. The potentiation was reversible and in the case of nicotine, no tachyphylaxis developed. The nicotine-induced potentiation was characterized by a rapid onset and an initial, transitory peak, while the enhancement caused by cocaine progressed more slowly and was monophasic. Hexamethonium and (+)-tubocurarine prevented the potentiation caused by nicotine. Nicotine did not prevent the adrenergic neurone blocking effect of bretylium on the response to field stimulation. Nicotine increased the stimulation-induced outflow of tritium from pulmonary artery preloaded with 3H-(--)-noradrenaline. Contractions of the artery elicited by tyramine were enhanced by pargyline, unaltered by nicotine and blocked by cocaine. Nicotine did not alter the concentration--response curve of exogenous (--)-noradrenaline while cocaine moved it to the left. The accumulation of 3H-(--)-noradrenaline by rabbit isolated aorta was not altered by nicotine, hexamethonium and (+)-tubocurarine. The accumulation of 3H-nicotine by the aorta was much lower than that seen with 3H-(--)-noradrenaline. The disposition of the 3H-nicotine accumulation into adventitia and media was concentration-independent. These results suggest (1) that nicotine potentiates the neurogenic vasoconstriction response in part by increasing the stimulation-induced release of transmitter from adrenergic neurone terminals; (2) that the site of the nicotinic receptors mediating this action is located on the outer surface of the neurones; and (3) that the potentiation is not due to blockade of noradrenaline re-uptake.

Animals↗
PubMed1979

Evidence for a noncholinergic site for nicotine's action in brain: psychopharmacological, electrophysiological and receptor binding studies.

In an effort to investigate the possibility of noncholinergic nicotine sites within the brain, psychopharmacological, biochemical and eletrophysiological studies were undertaken with nicotine and various newly synthesized derivatives of nicotine and piperidine. When 1-10 micrograms of (-)-nicotine was injected into the region of the lateral ventricle of rats through implanted cannulae, there resulted a characteristic prostration immobilization syndrome, which was accompanied by seizures and tremors at the higher dose range. The (+)-isomer possessed 1/100 the activity of the natural (-)-isomer. The syndrome could be prevented by pre-treatment, intraventricularly, with the N-benzyl and N-p-nitrophenylazido derivates of either nicotine or piperide. A variety of neurotransmitters and psychotropic agents, including acetylcholine and anticholinergic drugs, were without antagonistic action. After nicotine, recordings of spontaneous electrical activity from electrodes chronically implanted into the region of the dorsal hippocampus showed a marked decrease in the amplitude and number of 6-8 sec discharges, and the change was correlated with the behavioral syndrome. Receptor binding studies were performed with rat brain slices and various neural preparations using 3H-nicotine, 125I-alpha-bungarotoxin and 14C-d-tubocurarine as ligands; and only with 3H-nicotine was it possible to demostrate any competitive effect with the various nicotine and piperidine antagonists. It was possible to demonstrate stereospecific or specific nicotine binding to only glass fiber filters and, to a lesser extent, brain slices, but not to cell-free preparations. It was concluded that there existed specific noncholinergic sites for nicotine's action which have not been hitherto described.

Animals↗
PubMed1979

Nicotinic cholinergic receptors in brain synaptosomes.

In order to elucidate pharmacological characteristics of nicotinic receptors in the brain, competitive binding of nicotine analogues or cholinergic agents to brain particles was studied utilizing [3H]nicotine. The binding of [3H]nicotine to brain crude nitochondrial or synaptosomal fraction was progressively inhibited by the addition of increasing amounts of native nicotine or nornicotine, but cotinine had little effect. Of the myelin, synaptosomal and mitochondrial subfractions of the crude mitochondrial fraction, [3H]nicotine binding was almost exclusively confined to synaptosomes. In this binding, the affinity constant was 1.97 X 10(9)/M and the maximum binding capacity was 7.30 X 40(-8) M/g of protein. This binding was reduced by 50% in the presence of 4 X 10(-7) M D-tubocurarine and 10(-6) M carbamylcholine, while atropine was the least effective of the drugs tested. These findings suggest the possible existence of nicotinic cholinergic receptors in the synaptic region. A study of regional differences in nicotinic cholinergic receptors showed that higher specific bindings of nicotine to synaptosomes occurred in the hypothalamus, hippocampus and thalamus. These findings suggest that the nicotinic cholinergic mechanism plays an important role in these regions of the central nervous system.

Animals↗
PubMed1976

Reactions to cigarettes as a function of nicotine and "tar".

Experiments carried out to examine the effects of nicotine and "tar" on the extent of and subjective reactions to cigarette smoking. It was confirmed that smokers rate commercial, low-nicotine cigarettes as less "strong" and less "satisfying" than their usual brands. Since such cigarettes deliver reduced amounts of tar as well as of nicotine, an experiment to distinguish between the two was carried out with special cigarettes. Ratings of "strength" were directly related to nicotine but were not affected by tar. The numbers of cigarettes smoked fell slightly as their estimated delivery of nicotine increased, but tar had no effect on this index. The urinary excretion of nicotine was correlated with the rated yields of nicotine for the different cigarettes, but there was also evidence that subjects tended to adjust their manner of smoking so as to titrate their doses of nicotine. The results are interpreted as indicating a role for nicotine, but not for tar, in the maintenance of cigarette smoking behavior, and as support for the view that less harmful cigarettes should have a high yield of nicotine relative to tar.

Adult↗
PubMed1979

Effect of pH and urine flow on urinary nicotine excretion after smoking cigarettes.

Effects of pH and urine flow on urinary excretion of nicotine were examined in 11 smokers after they had smoked 3 cigarettes during water diuresis. Plasma nicotine showed a slight but nonsignificant rise after smoking. Urinary excretion of nicotine increased significantly from the pre-smoking levels of 258 +/- 76 and 252 +/- 147 (mean +/- SEM) ng/15 min to the peaks of 2,587 +/- 1,224 and 2.561 +/- 584 ng/15 min 30 and 45 min after the start of smoking. Thereafter, urinary nicotine tended to decrease and rise with changes in urinary flow. There was a correlation between urinary nicotine and urinary flow after smoking (r = 0.26, p less than 0.05). Eleven subjects were grouped based on the mean urinary pH throughout the experiment. No significant amount of nicotine was excreted in the group with pH above 7.5 while groups with pH below 7.4 excreted substantial nicotine after smoking. There was a negative correlation between urinary pH and nicotine excretion (r = -0.58, p less than 0.001). Urinary excretion of nicotine cannot be used as an index of smoking unless pH and urine flow are controlled.

Adult↗
PubMed1977

Nicotine chewing gum as a substitute for smoking.

The capacity of nicotine-containing chewing gum to produce plasma nicotine levels comparable to heavy cigarette smoking was tested in 21 subjects. On a fixed schedule of one piece of gum (4 mg nicotine) per hour, the average peak plasma nicotine concentration was 175-7 nmol/l (28-5 ng/ml) compared to 189-3 nmol/l (30-7 ng/ml) obtained from normal ad libitum smoking. Unpleasant side effects were common and in some cases plasma nicotine concentrations were two and even three times as high as with smoking; The chewing gum provided some satisfaction to all but four subjects, but its degree was not related to the concentration of plasma nicotine it produced, neither was there an inverse relation between the plasma nicotine concentration while taking the gum and the subjective sense of missing cigarettesmthis suggests that the capacity of the gum to act as a substitute for smoking is not necessarily related to its capacity to provide nicotine. Flexible dosage dictated by individual needs would probably lower the incidence of side effects and might secure closer approximation to smoking concentrations of plasma nicotine.

Adult↗