Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0406810 (NAME)
 13,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rats pretrained in a conditioned avoidance (CAR) paradigm were put on eight potentially addictive drugs in drinking water at two dose levels each. Fluid intake and body weight, monitored during the drugged (addiction) and nondrugged (withdrawal) states, showed drug/dose-dependent fluctuations in most groups. Extinction and relearning trials were spread over both drug and nondrug phases. CAR-performance generally deteriorated in the early drug phase but improved to near normalcy during the late drug and withdrawal phases in all groups except for alcohol and barbiturate-treated one. Excluding amphetamine, low-dose morphine and phenobarbital groups, substantial extinction of CAR occurred during the drug phase only; these three groups, as well as the high-dose alcohol, barbiturates and medazepam ones, showed extinction during the nondrug phase also. The rate and extent of a second-order relearning neither differed significantly between the groups nor was truly contingent upon prior extinction. These results are discussed in the light of state-dependent learning, comparing them with those from another series of rats primarily trained under the influence of these addictive drugs.
Physiol Behav 1975 Sep
PMID:Conditioned avoidance behavior in pretrained rats intermittently treated with addictive drugs. 123 80

The present studies were performed in order to examine the possible role of cyclic GMP-stimulated phosphodiesterase (cGMP-PDE) activity in the inhibitory action of the inflammatory peptide bradykinin on cyclic AMP (cAMP) accumulation in D384 cells. Bradykinin decreased the forskolin-stimulated cAMP accumulation in the presence of the phosphodiesterase inhibitor rolipram, and caused a transient 50% rise in cellular cGMP in the presence of the nonselective PDE inhibitor 3-isobutyl-1-methylxanthine (IBMX). Both basal and bradykinin-stimulated cGMP accumulation were about 8 times higher in the presence of IBMX than in the presence of rolipram. Sodium nitroprusside, which caused a 20-70-fold increase in cGMP levels reduced forskolin stimulated cAMP accumulation, whereas hydroxylamine, which maximally caused a 16-fold increase in cGMP, did not. 8-bromo-cGMP or dibutyryl cGMP had no effect on cAMP accumulation induced by forskolin. The inhibitory effect of nitroprusside was totally reversed by blocking the soluble guanylate cyclase activity by methylene blue treatment; however, the inhibitory action of bradykinin on cAMP accumulation was not changed by this treatment. Additionally, inhibition of nitric oxide synthesis, which is known to be regulated by Ca2+ and in turn stimulates cGMP production, by N omega-nitro-L-arginine (L-NAME) treatment did not alter the inhibitory effect of bradykinin on forskolin-induced cAMP accumulation. These results indicate that large increases in cGMP may regulate cAMP via cGMP-PDE whereas the small increase induced by bradykinin is insufficient and that cGMP is not involved in the inhibitory action of bradykinin on cAMP levels in D384 cells.
Neurochem Int 1992 Sep
PMID:Bradykinin inhibition of cyclic AMP accumulation in D384 astrocytoma cells. Evidence against a role of cyclic GMP. 128 20

L-NAME (Nw-Nitro-L-arginine methylester) and L-NMMA (NG- Monomethyl-L-arginine, monoacetate) are used widely as nitric oxide (NO) synthase inhibitors. Because of their functional groups (alcohols, amines and carboxylates), it appeared that they could interact with iron in a variety of systems. Using three in vitro models we observed these two compounds had inhibitory effects on cytochrome C reduction by ferrous iron, by ferrous iron accelerated by an unsaturated fatty acid or by epinephrine. This suggests that L-NAME and L-NMMA could have effects in iron containing systems found intracellularly apart from their inhibition of (NO) synthesis.
Biochem Biophys Res Commun 1992 Sep 16
PMID:The non specificity of specific nitric oxide synthase inhibitors. 138 21

An in vitro model has been developed in which the acute development of collateral perfusion of a segment of rabbit central ear artery, isolated between ligatures, is assessed by X-ray microangiography. Collateral perfusion was quantified by normalizing the volume of the segment filled with respect to its preocclusion control. The influence of endothelium-derived relaxing factor (EDRF) activity on perfusion was examined by using 100 microM NG-nitro-L-arginine methyl ester (L-NAME), a potent inhibitor of nitric oxide synthesis. Filling of the isolated segment after occlusion was time dependent, being 21.6 +/- 4.2% after 2 min and 46.6 +/- 5.3% after 90 min. This acute development of collateral flow was reversed by addition of L-NAME 60 min after ligation, after which filling was reduced to 17.8 +/- 3.8%. When L-NAME was added before ligation, filling of the segment was 15.6 +/- 5.9% at 2 min and 14.8 +/- 7.4% at 90 min, so that the time-dependent component of collateral flow development was abolished. The inhibitory effects of L-NAME on collateral perfusion were reversed by an excess of L-arginine. These findings indicate that EDRF plays a central role in the development and maintenance of collateral flow.
Am J Physiol 1992 Sep
PMID:EDRF plays central role in collateral flow after arterial occlusion in rabbit ear. 141 99

1. The present study was performed to investigate how blockade of the L-arginine/nitric oxide (NO) pathway influences the function of the lower urinary tract in vivo, as studied by cystometry in conscious rats and in vitro, in isolated muscle preparations from the rat detrusor and urethra. 2. L-NG-nitro arginine methyl ester (L-NAME), 10 and 20 mg kg-1, administered intra-arterially, decreased micturition volume and bladder capacity, and increased spontaneous bladder contractions. D-NAME (20 mg kg-1) had no effect. No changes in the urodynamic parameters were recorded if L-NAME (20 mg kg-1) was administered in combination with L-arginine (200 mg kg-1). 3. Cystometries performed after intra-arterial administration of sodium nitroprusside (SNP) (3 mg kg-1) and 3-morpholino-sydnonimin hydrochloride (SIN-1, 2 mg kg-1) showed a decrease in bladder capacity, micturition volume and threshold pressure. SIN-1, but not SNP, induced spontaneous bladder contractions. 4. Isolated precontracted urethral preparations responded to electrical stimulation with a frequency-dependent tetrodotoxin-sensitive relaxation. L-NAME (10(-4) M), but not D-NAME, reduced the maximal relaxation to 31 +/- 8% (n = 8) of the response prior to drug administration. The inhibition induced by L-NAME was completely reversed by L-arginine (10(-3) M). SNP (10(-8)-10(-4) M), SIN-1 (10(-6)-3 x 10(-4) M) and NO (10(-5)-10(-3) M; present in acidified solution of NaNO2), caused relaxation (93-100%) of urethral preparations. L-NAME did not affect these relaxations.5. Detrusor strips contracted by carbachol or K' showed contractions in response to electrical stimulation, even when pretreated with a,p-methylene ATP and/or atropine. Small relaxations (14-41%) of detrusor strips were evoked by SNP (10-6-10-4M), SIN-1 (10-5-3 x 10-4M) and NO (10-5-10-3M). Electrically (20 Hz) induced contractions of the detrusor muscle were unaffected by addition of L-NAME (10-6_10-4 M) or L-arginine (10-3 M).6. The present results suggest that the L-arginine/NO pathway is of functional importance for the bladder outlet region, but that its role in the detrusor is questionable. They also suggest that the site of action of L-NAME for inducing bladder hyperactivity in the rat is the outlet region rather than the detrusor muscle.
Br J Pharmacol 1992 Sep
PMID:Effects of inhibition of the L-arginine/nitric oxide pathway in the rat lower urinary tract in vivo and in vitro. 142 71

Our previous studies have shown that endothelin-1 (ET-1) induces an initial relaxation followed by a contraction in the guinea-pig ileum. To test whether other ET isopeptides (ET-2, ET-3, vasoactive intestinal contractor (VIC) and sarafotoxin S6b) and big ET-1, the ET-1 precursor, also induce similar biphasic responses, we compared their effects in isolated guinea-pig ileum. In addition, the mechanism of initial relaxation was studied. At 1-100 nM, ET-1, ET-2 and VIC were equipotent in producing the biphasic responses. S6b also produced similar biphasic responses, except that only a relaxation was elicited at 1 nM. ET-3 was approximately 30- to 100-fold less active than ET-1 in producing the contraction, whereas it was as potent as ET-1 in producing relaxation. Big ET-1 induced a relaxation of slower onset and longer duration, followed by a weak contraction at concentrations higher than 30 nM. The initial relaxation produced by ET-1 was not affected by pretreatment with L-NAME (NW-nitro-L-arginine methyl ester), hemoglobin, 9-AC (anthracene-9-carboxylic acid), SITS (4-acetamido-4'-isothiocyanatostilbene-2-2'-disulfonic acid), glibenclamide, ouabain, phorbol 12,13-dibutyrate, sodium nitroprusside, human atrial natriuretic peptide (hANP) or forskolin, whereas it was abolished by pretreatment with apamin. Although phorbol 12,13-dibutyrate pretreatment had no significant effect on the biphasic response of ET-1, it rapidly reversed the sustained contraction produced by ET-1. These results indicate that the initial relaxation is caused by the activation of Ca(2+)-activated K+ channels.
Eur J Pharmacol 1992 Sep 04
PMID:Intestinal relaxation by endothelin isopeptides: involvement of Ca(2+)-activated K+ channels. 142 64

The efficacy of three selective broths and agars, i.e. Preston-, mCCD- and CAR medium, were compared to each other in various combinations. Twelve Campylobacter coli and 9 Campylobacter jejuni strains that had been isolated from sewage were used as test strains. To evaluate the applicability for highly contaminated environmental samples 15 sewage samples were examined, subsequently. Significant differences between the media could not be ascertained. The application of Preston broth/agar or CAR broth/Preston agar, however, is strongly recommended for investigation of highly contaminated environmental samples, as bacterial overgrowth (CAR agar) and difficult retrievability from agar surfaces (mCCD agar) were observed. A necessity of blood-supplementation is assumed.
Zentralbl Hyg Umweltmed 1991 Sep
PMID:A note on the comparative efficacy of three selective media for isolation of Campylobacter species from environmental samples. 175 Sep 64

1. The role of endothelial nitric oxide synthesis from L-arginine in the regulation of coronary vascular tone and myocardial tissue perfusion was evaluated in anaesthetized, open-chest dogs. Coronary blood flow was measured with an electromagnetic flow probe placed around the left circumflex coronary artery. Coronary vascular resistance was calculated from mean arterial blood pressure and mean coronary blood flow, whereas regional myocardial tissue flow was determined by use of the radioactive microspheres technique. 2. NG-monomethyl L-arginine (L-NMMA) and NG-nitro-L-arginine methyl ester (L-NAME), administered directly into the left circumflex artery, induced a small increase in arterial blood pressure and an increase in coronary vascular resistance. However, myocardial tissue perfusion, assessed by the microspheres technique (whether subendocardial, subepicardial, or transmural), was unaffected by L-NMMA or L-NAME. 3. Acetylcholine, administered intracoronarily, induced an increase in left circumflex coronary blood flow and a decrease in coronary vascular resistance, without affecting systemic haemodynamics. This coronary vasodilator effect of acetylcholine was markedly inhibited by L-NMMA and L-NAME, the latter being a more potent antagonist than the former. 4. These results indicate that the endothelial L-arginine pathway is largely responsible for the coronary vasodilator effect of acetylcholine. However, although basal release of nitric oxide from L-arginine apparently contributes to the regulation of resting coronary vascular tone, blockade of this pathway does not affect myocardial tissue perfusion, possibly because of compensatory mechanisms occurring at the level of small arterioles and/or capillaries.
Br J Pharmacol 1991 Sep
PMID:Regional coronary haemodynamic effects of two inhibitors of nitric oxide synthesis in anaesthetized, open-chest dogs. 178 19

In Carney's syndrome, the association of cardiac myxomas, spotty pigmentation and endocrine over activity, the myxomas are usually multiple and have atypical locations. The authors report a case in which an accurate diagnosis of these multiple myxomas was made by transoesophageal echocardiography, although transthoracic echocardiography had missed the diagnosis.
Arch Mal Coeur Vaiss 1991 Sep
PMID:[Echocardiographic aspects of multiple myxoma in Carney's syndrome]. 195 21

The topography and functional domains of the cAMP chemotactic receptor of Dictyostelium discoideum were investigated by protease sensitivity to chymotrypsin. Proteolytic digestion of intact cells produced a 23-kDa fragment of the receptor that retained the photoaffinity label used to identify the receptor. Additionally, this fragment contained the sites phosphorylated by CAR-kinase, the enzyme that phosphorylates the ligand-occupied form of the receptor. The fragment was also found to be phosphorylated in response to cAMP stimulation of cells. Proteolytic digestion of either intact cells or membrane preparations did not appreciably alter the binding properties of the receptor, indicating that the domains which determine the cAMP binding pocket are likely to be transmembrane regions of the protein. Additionally, the sensitivity of down-regulated receptors to chymotrypsin digestion suggests that the initial loss of cAMP binding activity upon incubation of cells with high concentrations of ligand does not require receptor internalization.
J Biol Chem 1990 Sep 15
PMID:Localization of functional domains of the cAMP chemotactic receptor of Dictyostelium discoideum. 220 80


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