Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:EXPT02427 (Atropine)
 3,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The MK-801-induced hyperactivity in rats was antagonized by haloperidol and, to a lesser degree, by SCH 23390, a dopamine D-1 antagonist, and sulpiride, a dopamine D-2 antagonist. Combined treatment with MK-801 + D-amphetamine, or MK-801 + apomorphine caused a stronger locomotor hyperactivity than each of those drugs given alone. The stereotypy evoked by D-amphetamine or apomorphine was not changed by MK-801. Atropine potentiated the effect of MK-801. Prazosin, idazoxan or ritanserin did not affect the MK-801-induced hyperactivity. It was reduced by pretreatment with alpha-methyl-p-tyrosine (alpha-MT) and completely abolished by pretreatment with reserpine, or with reserpine+alpha-MT. Also combined administration of MK-801 + clonidine increased the activity of rats pretreated with reserpine+alpha-MT. Our results indicate that the dopamine system is mainly involved in the locomotor hyperactivity induced by MK-801.
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PMID:Locomotor hyperactivity induced by MK-801 in rats. 168 44

Autonomic receptor modulation of ultradian oscillations of blood pressure and heart rate was studied in telemetered free-running dogs. Data, analyzed for their harmonic content by fast Fourier transform (FFT) methods, indicated that ultradian and circadian oscillations of 22.9 +/- 2.5 and 10.5 +/- 0.9 (SD) mmHg, respectively, were present. The average principal frequency for the ultradian oscillations in 12 dogs was 0.760 +/- 0.11 cycles/h for arterial pressure and 0.808 +/- 0.10 for heart rate. Atropine had no effect on periodicity of either arterial pressure or heart rate. Metoprolol, a beta 1-antagonist, or hexamethonium, a ganglionic blocker, significantly reduced the power of both arterial pressure and heart rate (P less than 0.05), whereas the primary frequencies of both were unchanged. Prazosin, an alpha 1-blocker, sharply reduced arterial pressure power (P less than 0.05) and increased the power of heart rate (P less than 0.05), demonstrating that it is possible to uncouple arterial pressure oscillations from influences of heart rate. We conclude that the sympathetic limb of the autonomic nervous system is primarily responsible for these oscillations and that vagal influences on the heart partially dampen these rhythms.
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PMID:Autonomic modulation of ultradian blood pressure and heart rate oscillations in dogs. 256 83

Xylazole (Xyl) is an analogue of xylazine (Xyn) synthesized by Lanzhou Institute of Chinese Traditional Veterinary Medicine. The effects of Xyl on heart rate and blood pressure were studied in 5 conscious dogs. Xyl 1 mg/kg iv was similar to Xyn in producing bradycardia and an initial transient hypertension followed by a lasting hypotension which was less significant than Xyn. Yohimbine (0.1 and 0.3 mg/kg), an alpha 2-adrenoreceptor blocking agent, antagonized bradycardia and hypotension induced by Xyl. Tolazoline (3.3 mg/kg), a nonselective alpha-adrenoreceptor blocking agent, reversed the bradycardia and hypotensive effect. Prazosin (1 mg/kg), an alpha 1-adrenoreceptor blocking agent, did not change Xyl-induced bradycardia and hypotension. Atropine (20 micrograms/kg) not only antagonized Xyl-induced bradycardia but also changed from bradycardia to tachycardia, and greatly potentiated Xyl-induced hypertension for more than 30 min. The results suggested that Xyl-induced cardiovascular effects are similar to Xyn that mediated by alpha 2-adrenoreceptor.
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PMID:[Effects of xylazole on heart rate and blood pressure in conscious dogs]. 257 38

Halothane, in anesthetic concentrations (0.6-1.8 volumes/100 ml), produced a dose-dependent decrease in myocardial cyclic AMP (cAMP) content and an increase in cyclic GMP (cGMP) content in mice exposed to a continuous flow of the anesthetic carried in air for 15 min. Atropine (up to 20 mg/kg i.p.) did not alter significantly the myocardial cyclic nucleotides content or the effect of halothane on cAMP and cGMP content. Prazosin and yohimbine had no significant effect on cAMP or cGMP content in the absence of halothane. Both alpha adrenergic antagonists inhibited the halothane-induced increase in cGMP content (ID50, 0.24 and 0.54 mumol/kg i.p. for prazosin and yohimbine, respectively). In contrast, the decrease in cAMP content induced by halothane was not altered by alpha adrenergic antagonists. Propranolol (2 mg/kg i.p.) diminished myocardial cAMP level and prevented the halothane effect on myocardial cAMP content. Pretreatment with 6-hydroxydopamine did not change the cGMP response to halothane. Thus, the action of halothane on myocardial cyclic nucleotides content appears to be predominantly a peripheral effect, not related to cellular mechanisms mediated by muscarinic receptors. The results suggest that the increase in cGMP content induced by halothane does not require intact adrenergic nerve endings and that cellular processes associated with the alpha adrenoceptor system may be involved; the decrease in cAMP content may be due to an inhibition of the beta stimulatory action of catecholamines on adenylate cyclase.
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PMID:Effect of halothane on myocardial cyclic AMP and cyclic GMP content of mice. 286 13

1. The present study was to ascertain whether drugs cause differential antagonism of the initial fast and secondary slow contractile responses to phenylephrine, 5-HT and methacholine of the rat portal vein. 2. Cocaine (5 x 10(-6) M) had no effect on the responses to methacholine. Cocaine potentiated the initial fast but not the secondary slow responses to phenylephrine suggesting that neuronal uptake limits the initial fast but not the secondary slow response to phenylephrine. Cocaine reduced the maximal responses to 5-HT suggesting that the responses to high concentrations of 5-HT are due, in part, to the release of noradrenaline. 3. In the presence of cocaine, idazoxan had no effect on responses to phenylephrine or 5-HT and prazosin had no effect on responses to 5-HT. Prazosin (3 x 10(-9)-10(-8) M) inhibited the responses to phenylephrine causing similar parallel rightward shifts of the concentration-response curves to the initial fast and secondary slow responses. 4. In the presence of cocaine, mianserin (10(-9)-10(-8) M), cyproheptadine, (10(-10)-10(-9) M), methysergide (10(-8) M), ketanserin (10(-10)-10(-9) M) and Ly 53857 (at 10(-9)-10(-8) M) had similar inhibitory effects on the initial fast and secondary slow responses to 5-HT, namely a parallel rightward displacement of the concentration-response curves. 5. Atropine (less than or equal to 10(-7) M) and pirenzepine less than or equal to 10(-6) M) had no effect on the responses to phenylephrine and 5-HT, but caused similar parallel rightward shifts of the concentration-response curves to both responses to methacholine. 6. The results of this study provide no evidence for differential antagonism of the initial fast and secondary slow responses of the rat portal vein to phenylephrine, 5-HT or methacholine.
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PMID:No evidence for the differential antagonism of the initial fast and secondary slow contractile responses of the rat portal vein to phenylephrine, 5-hydroxytryptamine or methacholine. 290 98

Leucine-enkephalin (Leu5-ENK) (35 micrograms/kg) increased heart rate and mean systemic arterial blood pressure following intravenous injection into chronically-instrumented, conscious dogs. Repeated injections at five-minute intervals were not associated with a diminished response. Naloxone (1 mg/kg) pre-treatment inhibited both heart rate and blood pressure increases. Prazosin (1 mg/kg) attenuated the increase in blood pressure but did not influence the heart rate response. Propranolol (1 mg/kg) attenuated the heart rate response but not the pressor response. Clonidine (30 micrograms/kg) attenuated the positive chronotropic effect of Leu5-ENK. Atropine (1 mg/kg) plus propranolol (1 mg/kg) blocked the heart rate response but the pressor effect was still present. The attenuation of the heart rate response by propranolol and the pressor response by prazosin suggests an adrenergic component to the enkephalin response; the reduction in the heart rate response by clonidine and atropine-propranolol indicates a role for cholinergic mechanisms in the chronotropic response. Hexamethonium (10 mg/kg) blocked the heart rate response and markedly inhibited the pressor response. Vagal interruption attenuated both heart rate and blood pressure responses. It is concluded that intravenous Leu5-ENK stimulates afferent pathways located in fibers which are contained in the vagosympathetic trunk to reflexly increase heart rate and blood pressure.
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PMID:Mechanism of the cardiovascular response to systemic intravenous administration of leucine-enkephalin in the conscious dog. 613 9

The responses of the bovine retractor penis muscle to field stimulation of intramural nerves in vitro was investigated using micro-electrode and extracellular (sucrose gap) techniques. In the absence of tone single pulses or trains of stimuli (1-50 Hz 0.1-0.5 m.sec) produced e.j.p.s and a decrease in membrane resistance; spike potentials were not observed. E.j.p.s often small in amplitude (3-5 mV to single pulse) and accompanied by contractions in almost all preparations were noradrenergic, abolished by guanethidine (1-3 x 10(-5) M) and tetrodotoxin (3.5 x 10(-6) M) but not by prazosin (0.05 - 1.4 x 10(-6) M). Prazosin abolished the depolarization and contraction produced by added NA (0.02 - 2 x 10(-8) moles). TEA (10(-2) M) depolarized the membrane and initiated spontaneous activity; e.j.p.s and contractions were enhanced and prolonged but no spikes were observed. Atropine (0.5 x 10(-6) M) increased and physostigimine (1-5 x 10(-6) M) decreased e.j.p.s and contractions indicating a cholinergic regulatory component in the release of the excitatory transmitter. In the presence of tone, nerve stimulation produced i.j.p.s. and relaxations which were unaffected by apamin (5 x 10(-7) M), atropine (3 x 10(-6) M), guanethidine (3 x 10(-5) M), phentolamine (5 x 10(-6) M) and propranolol (4 x 10(-6) M) but were abolished by tetrodotoxin (3.5 x 10(-7) M) suggesting their mediation by non-adrenergic non-cholinergic (NANC) nerves. Sodium nitroprusside (10(-10) - 10(-8) moles), which increases cyclic GMP, also hyperpolarized the membrane and relaxed the BRP. Those responses and those to inhibitory nerve stimulation were antagonized by oxyhaemoglobin which inhibits guanylate cyclase. 2-O-propoxyphenyl-8-azapurin-6-one (M & B 22948 3-9 x 10(-6) M) which inhibits cGMP-specific phosphodiesterase, enhanced the relaxation but not the i.j.p. TEA (10(-2) M) initially depolarized the membrane potential and raised tone. In the sucrose gap inhibitory potentials were abolished; the mechanical relaxation was not and a small contractile component emerged. Electrical and mechanical inhibitory components in the bovine retractor penis may not be correlated.
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PMID:Electrical and mechanical responses of the bovine retractor penis to nerve stimulation and to drugs. 615 68

Prazosin, haloperidol, propranolol or timolol had no effect on the electrically evoked muscular twitch. Atropine was able to antagonize competitively acetylcholine (pA2 = 9.29 +/- 0.30). The muscular twitch of the Octodon degus vas deferens was only partially abolished by atropine (53.2 +/- 0.72). The present results can be interpreted assuming that the Octodon degus vas deferens has one component muscarinic in its innervation.
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PMID:Cholinergic transmission in vas deferens. 631 25

Clonidine (10(-9)-3 X 10(-6) M) produced a concentration dependent inhibition of field stimulation-induced contractions of rat detrusor muscle strip at 0.1 and 1 Hz which were completely abolished by tetrodotoxin (5 X 10(-7) M) but were unaffected by hexamethonium (10(-5) M). Pretreatment with yohimbine (10(-8)-10(-7) M) did not modify the amplitude of contractions but produced a rightward parallel shift of clonidine's cumulative response curve without a depression of the maximal response. The corresponding pA2 value for yohimbine was 8.44 +/- 0.1. Atropine (3 X 10(-6) M) produced a partial inhibition of contractions at both frequencies. In the presence of atropine the cumulative response curve of clonidine was significantly reduced at 1 but not at 0.1 Hz. Indomethacin (5 X 10(-5) M) and theophylline (2 X 10(-4) M) produced a partial inhibition of amplitude of contractions at both frequencies without any interference with the effect of a supramaximal concentration of clonidine. Prazosin (10(-6) M), propranolol (10(-6) M), chlorpheniramine (10(-6) M), ranitidine (10(-6) M), haloperidol (10(-7) M), pizotifen (10(-6) M), naloxone (10(-6) M), quinidine (10(-6) M), strychnine (10(-5) M) or picrotoxin (10(-5) M) neither affected the amplitude of contractions at either frequency nor antagonized clonidine effects. The contractile response of non stimulated strips to acetylcholine (10(-5) M), carbachol (3 X 10(-6) M) and ATP (10(-3) M) were not significantly influenced by pretreatment with clonidine (3 X 10(-6) M). These results suggest that stimulation of prejunctional alpha 2-adrenoreceptors located on postganglionic nerve endings might reduce the output of excitatory neurotransmitter(s) in rat urinary bladder.
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PMID:The effects of clonidine on electrically-induced contractions of rat detrusor strips in vitro. 664 49

Intravenous administration of St 91 (2-(2,6-diethylphenylimino)-imidazolidine hydrochloride) (8 and 16 micrograms/kg) to anaesthetized cats, produced a dose-related but brief rise in blood pressure accompanied by bradycardia. The bradycardia was biphasic. An initial rapid fall in heart rate accompanied the pressor response and was followed by a less pronounced residual bradycardia that long outlasted the pressor response. Prazosin (5 micrograms/kg i.v.) reduced both the mean resting blood pressure and the maximum pressor response to St 91 (8 and 16 micrograms/kg i.v.) and unmasked a small secondary hypotension. The bradycardia was not diminished. Atropine (1 mg/kg i.v.) did not alter the pressor response to St 91 (16 micrograms/kg i.v.) but depressed the initial bradycardia accompanying the pressure rise. The residual bradycardia was not reduced. Piperoxan (150 micrograms/kg i.v. or 10 micrograms/kg i.a. vert.), given after St 91 (16 micrograms/kg i.v.) abolished the residual bradycardia whereas pretreatment with piperoxan (150 micrograms/kg, intracisternally) inhibited both the initial and the residual bradycardia. St 91 (8 and 16 micrograms/kg i.a. vert.) caused hypotension and bradycardia. Prazosin (5 micrograms/kg i.a. vert.) inhibited the hypotension only, but the same dose i.v. was ineffective. Piperoxan (150 micrograms/kg i.v. or 10 micrograms/kg i.a. vert.) given 15 min after St 91 (16 micrograms/kg i.a. vert.) reduced both the hypotension and bradycardia. The results show that the long-lasting residual bradycardia caused by i.v. St 91 is due to activation of central alpha-adrenoceptors. Selective inhibition of the St 91 (i.a. vert.) hypotension by prazosin may indicate that different receptors mediate hypotension and bradycardia but more likely shows that the central pathways differ.
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PMID:Effects of prazosin and piperoxan on central cardiovascular actions of St 91 in cats. 716 Apr 31


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