Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1323099 (sympathomimetic)
 2,957 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nicotine (0.14--0.25 mg/kg), injected intravenously or intraarterially into conscious pregnant ewes, caused a decrease in fetal PaO2 within 5 minutes, persisting for up to 30 minutes. There was a significant fall in the incidence of fetal breathing movements. These changes did not occur if the ewe was treated with an alpha-blocking agent (phentolamine) or if the nicotine was infused for 30 minutes at 0.27 to 0.85 mg/minute. Nicotine crossed the placenta; fetal concentrations equaled those in the ewe 5 minutes after the injection and remained at or above maternal levels for 1 hour. Nicotine given directly to the fetus (0.005--0.03 mg/kg estimated fetal weight) stimulated fetal breathing movements in a dose-related manner. We suggest that the maternal injection of nicotine results in a fall of uterine blood flow by a sympathomimetic action, leading to transient fetal hypoxemia and a reduction of fetal breathing movements and that a similar phenomenon may occur when a pregnant woman smokes cigarettes.
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PMID:The effect of nicotine on fetal breathing movements in conscious pregnant ewes. 3 87

Spontaneous electrical activity, recorded extracellularly from the sinoatriial pacemaker region in the isolated chick embryo heart, was inhibited by nicotine (10(-5)M) on the 11th incubation day and thereafter. Blockade of the inhibitory effects of nicotine hexamethonium, tetroditoxin and atropine supported the conclusion that nicotine initiated propagated impulses in postganglionic cholinergic nerves and released acetylcholine to act on atropine-sensitive receptors on pacemaker cells. Dimethylphenylpiperazinium, like nicotine, inhibited the sinoatrial pacemaker. The onset of the inhibitory effect of nicotine occurred within 1 day of the appearance of cholinergic neuroeffector transmission. The acceleratory action of tyramine (2.9 X 10(-5)M) increased markedly on the 20th incubation day, that is, within 1 day of the appearance of adrenergic neuroeffector transmission. The positive chronotropic effects of tyramine were opposed by cocaine and by propranolol. Nicotine also evoked pacemaker acceleration that was observed on the 21st incubation day and thereafter. However, the sympathomimetic effect of nicotine required elevation (2 times normal) of the external Ca++ concentration. Ontogenetic and pharmacologic evidence support the conclusion that the drug-induced changes in pacemaker impulse frequency depended upon an interaction with autonomic nerves. The results are consistent with the hypothesis that the gap between morphologic innervation of the heart by autonomic nerves and the appearance of transmission is related, at least in part, to the amount of transmitter available for release.
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PMID:Onset of chronotropic effects of nicotinic drugs and tyramine on the sinoatrial pacemaker in chick embryo heart: relationship to the development of autonomic neuroeffector transmission. 17 54

Nicotine has a small molecular weight and is absorbed via the mucosa (Guccal or nasal), the pulmonary alveoli and the skin. The phenomenon of autotitration explains how a dependent smoker can unconsciously change his method of smoking to maintain a steady nicotine level. Nicotine leads to a liberation of catecholamines by acting on the nervous system through the intermediary of nicotine receptors. There is increased vigilance and powers of intellectual concentration, an awakening reaction and some anxiolytic and euphoriant effects. From the cardiac stand point there is an increased heart rate and blood pressure, as a result of the sympathomimetic effects. Elimination is via the kidneys as unchanged nicotine, cotinine and 1'-N-oxide of nicotine. Nicotine has an addictive action and is capable of inducing pharmacological dependency, tolerance and withdrawal syndrome in cases of abrupt cessation. A knowledge of the pharmacology of nicotine is important in the process of stopping smoking.
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PMID:[Pharmacology of nicotine]. 150 83

After refraining from smoking for at least 8 hours, 22 adult male habitual smokers underwent baseline electrophysiologic study including atrial and ventricular burst pacing and programmed premature stimulation with single extrastimuli. After smoking 2 of their usual brand of cigarettes in rapid succession, the electrophysiologic protocol was repeated. Nicotine, catecholamine and carbon monoxide concentrations all increased significantly. Smoking increased heart rate and improved atrioventricular conduction in the 13 patients receiving chronic beta-blocker therapy (mostly for angina pectoris); increases in heart rate and improvement in atrioventricular conduction were not different statistically from those seen in patients not receiving beta-blocker therapy, suggesting the possibility of a direct effect of nicotine or other components of tobacco smoke. Ventricular refractoriness was not altered and atrial and ventricular arrhythmias were not increased by smoking. Persistent sympathomimetic actions of cigarette smoking may explain in part the failure of beta-blocking drugs to reduce cardiac mortality risk in smokers after myocardial infarction.
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PMID:Electrophysiologic effects of cigarette smoking in patients with and without chronic beta-blocker therapy. 289 Feb 91

1. Nicotine produced a transient contraction of isolated strips of guinea-pig urinary bladder. The response to nicotine was antagonized by the nicotinic receptor antagonist, hexamethonium but was insensitive to tetrodotoxin. 2. The nicotine-induced contraction was potentiated by the cholinesterase inhibitor, physostigmine, and was reduced to 50% and 70% by the muscarinic cholinoceptor antagonist, atropine and the sympathetic neurone blocking drug, guanethidine, respectively. Chemical denervation with 6-hydroxydopamine abolished the inhibitory effect of guanethidine. Simultaneous treatment with atropine and guanethidine did not abolish the response to nicotine, but the degree of inhibition was comparable to that obtained with atropine alone. 3. The nicotine-induced contraction was insensitive to bunazosin and yohimbine (alpha 1- and alpha 2-adrenoceptor antagonists, respectively), and exogenously applied noradrenaline did not cause a contraction even in the presence of blockade of noradrenaline uptake mechanisms with desipramine and normetanephrine and of beta-adrenoceptors with propranolol, suggesting a non-adrenergic nature of the sympathomimetic effect of nicotine in this tissue. 4. The nicotine-induced contraction in the presence of atropine was abolished after desensitization of P2-purinoceptors with alpha, beta-methylene adenosine 5'-triphosphate, a slowly degradable ATP analogue selective for P2-purinoceptors. By this desensitization, the response to ATP, but not to histamine, was also abolished. 5. A cyclo-oxygenase inhibitor flurbiprofen partially inhibited the nicotine-induced contraction. The degree of the inhibition was more pronounced in the presence of atropine than in its absence. Flurbiprofen antagonized the response to exogenously applied ATP in an unsurmountable manner, but not that to carbachol. 6. The present results suggest that nicotine might induce a contraction through an interaction with nicotinic receptors located on the terminals of, possibly, (i) parasympathetic cholinergic, (ii) sympathetic non-adrenergic and (iii) non-sympathetic purinergic nerves in guinea-pig detrusor preparations, and that a portion of the contraction due to the purine nucleotide released is possibly potentiated by intramural prostaglandin(s). Parasympathetic cholinergic output might be modulated by an unknown excitatory substance released by nicotine from sympathetic nerve. 7. Nicotine reveals a latent excitatory effect of the sympathetic hypogastric nerve which innervates guinea-pig detrusor.
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PMID:Mechanism of action of nicotine in isolated urinary bladder of guinea-pig. 322 73

The effects of optically pure d-nicotine were investigated as compared with those of the l-isomer. d-Nicotine showed qualitatively the same effects as the l-isomer in the ganglionic or neuromuscular sites and the relative potency of the d-isomer was approximately 0.06 in the case of rat blood pressure (elevation), approximately 0.2 in the cat superior cervical ganglion (stimulation and blockade) and approximately 1.0 in the neuromuscular junctions of the rat diaphragm (blockade). In the adrenergic nerve terminals of the isolated rabbit pulmonary artery, l-nicotine produced sympathomimetic effects by releasing norepinephrine from those terminals. d-Nicotine, on the other hand, did not produce such effects, but instead inhibited those effects due to the l-isomer. Because d-nicotine had no effect on the response to exogenously applied norepinephrine and blocked the 3H-efflux induced by the l-isomer from the preparations preincubated with [3H]norepinephrine, the inhibitory effect of the d-isomer was attributed to its presynaptic action. Such an inhibitory effect of d-isomer was noncompetitive, on the basis of the shift of the concentration-contraction curve with the l-isomer. Simultaneous application of both isomers produced no inhibition of the response to the l-isomer, irrespective of the concentration of d-nicotine. Occurrence of the inhibitory effect of d-nicotine was not prevented by hexamethonium. d-Nicotine did not inhibit the responses of the artery to electrical transmural stimulation. These results indicate that d-nicotine inhibits the response to l-isomer by acting neither on the nicotinic receptors nor on excitation-secretion coupling mechanisms. Furthermore, such an effect of the d-isomer would be similar to that reported in the case of l-isomer, i.e., "nicotinic desensitization."
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PMID:The effects of d-nicotine and l-isomer on nicotinic receptors. 709 65

The possible involvement of sodium action potentials in sympathomimetic effects of nicotine was investigated using isolated guinea-pig aortas. Goniopora toxin (GPT), a polypeptide isolated from coral, was used to increase the sodium influx through the fast sodium channel of the postganglionic sympathetic nerves; tetrodotoxin (TTX) was used to block this flux. Nicotine (10-300 microM) produced sympathetic nerve-mediated contractions in a concentration-dependent manner. GPT (30 nM) enhanced the responses to nicotine over the entire range of concentrations tested, yet there was no effect on resting tension. Such an effect of GPT was concentration-dependent and was apparent in concentrations over 10 nM. GPT had no effect on the responses to exogenously applied norepinephrine. TTX (100 nM) abolished this potentiating effect of GPT, but did not inhibit the usual nicotine-induced responses. The 3H-efflux induced by nicotine (100 microM) in the preparations preincubated with [3H]norepinephrine was not significantly inhibited by TTX (100 nM). GPT (30 nM) markedly augmented nicotine-induced 3H-efflux and TTX prevented this effect of GPT. These results appear to indicate that the augmentation of the nicotine-induced response by GPT in isolated guinea-pig aortas is due to a prolongation of the duration of the presynaptic action potential. The effects of nicotine on adrenergic nerve terminals may involve two mechanisms, i.e.: 1) one mediated by sodium action potentials and 2) one independent of these action potentials.
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PMID:Nicotine-induced response in guinea-pig aorta enhanced by goniopora toxin. 714 40

The responses of the isolated rectum of the domestic chick (Gallus domesticus) to some drugs have been investigated. The tissue was found to be qualitatively and quantitatively similar to conventional mammalian gastrointestinal smooth muscles in its responses to pharmacological agents, and serves as a useful isolated smooth muscle preparation for investigating drug actions and interactions. Acetylcholine and its natural or synthetic analogues induced atropine-sensitive contractions of the tissue, while noradrenaline and other sympathomimetic drugs examined caused phentolamine-sensitive relaxations. 5-hydroxytryptamine contracted the tissue preparation, while histamine evoked a biphasic action (either a contraction or a relaxation, or even both occurring together one after the other). Potassium or barium ions contracted the muscle while magnesium ions relaxed it. Nicotine and dimethylphenylpiperazinium showed no effects on the muscle. The pharmacological implications of these findings are discussed. The receptor types present on the muscle have been classified as muscarinic cholinoceptors; histamine H1-and H2receptors; 5-hydroxytryptamine receptors, and alpha-adrenoceptors respectively.
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PMID:Studies on the responses of the isolated rectum of domestic chick (Gallus domesticus) to drugs. 734 58

1. Possible cholinoceptor-mediated effects on lipolysis were investigated in vivo in human subcutaneous adipose tissue of non-obese, non-smoking, healthy subjects, by use of microdialysis. Cholinomimetic and sympathomimetic agents were added to the in going dialysate solvent. 2. Addition of nicotine to the perfusion solvent caused a concentration-dependent reversible increase in the levels of glycerol in the dialysate (lipolysis index). The opposite effect (also concentration-dependent and reversible) was caused by the addition of carbachol. The maximum effects were 100% stimulation and 50% inhibition, respectively, by nicotine and carbachol. Neither nicotine nor carbachol stimulated nutritive blood flow in adipose tissue (as measured with an ethanol escape technique). 3. The nicotine effect in situ was concentration-dependently counteracted by the nicotinic cholinoceptor antagonist, mecamylamine. Likewise, the carbachol effect was concentration-dependently counteracted by the muscarinic cholinoceptor antagonist, atropine. 4. When adipose tissue was pretreated with phentolamine plus propranolol in order to obtain a complete alpha and beta-adrenoceptor blockade, the subsequent addition of nicotine or carbachol still induced an increase and decrease in dialysate glycerol levels (lipolytic or antilipolytic effects), respectively. When adipose tissue was pretreated with mecamylamine or atropine, the subsequent addition of acetylcholine caused a reversible decrease and increase, respectively, of the dialysate glycerol levels. 5. Nicotine and carbachol had no effects on glycerol release from human isolated subcutaneous fat cells that were incubated in vivo. 6. In conclusion, the data demonstrate a dual effect of the cholinoceptor system on glycerol output inhuman adipose tissue: stimulation through nicotinic receptors and inhibition through muscarinic receptors. These effects, which are not observed in vitro, are independent of the adrenergic system and the local blood flow and seem not to be mediated by a direct action on the fat cell.
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PMID:Cholinoceptor-mediated effects on glycerol output from human adipose tissue using in situ microdialysis. 758 38

Nicotine patch administration is often used to sustain tobacco abstinence in smoking-cessation programs. There is some concern regarding safety issues, as a consequence of the sympathomimetic action of nicotine. We used spectral analysis of RR interval and (noninvasive) systolic arterial pressure (SAP) beat-by-beat variabilities in a crossover double-blind design to assess the autonomic effects of cigarette smoking, of transdermal nicotine, and of placebo. The study group consisted of 27 heavy smokers (age 43 +/- 2 years). The RR interval and its variability were significantly reduced in the smoking group, as compared with nicotine or placebo groups. The LF component of RR interval variability (in normalized units, nu), and the LF/HF ratio showed greatest values during smoking, as compared with placebo. Values of LF(RR) and LF/HF during nicotine patch treatment were slightly, but not significantly, greater than observed with placebo. No differences were observed in SAP and its variability components. The index alpha (a frequency domain measure of baroreflex gain) was minimal in the smoking period. Habitual cigarette smoking is associated with signs of sympathetic predominance in the autonomic control of the sinoatrial (SA) node. Nicotine patches produce only minor disturbances of autonomic regulation. This corroborates their safe use in smoking-cessation strategies.
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PMID:Autonomic effects of nicotine patch administration in habitual cigarette smokers: a double-blind, placebo-controlled study using spectral analysis of RR interval and systolic arterial pressure variabilities. 959 71


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