Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.6.99.1 (NADPH-diaphorase)
 3,903 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Benzyldimethyltetradecylammonium chloride (BAC) has previously been used to create amyenteric rat jejunal models. Fifteen opossums (D. virginiana) were injected with 10-15 mL 4 mM BAC or saline in the distal oesophagus and along with controls underwent oesophagoscopy, manometry and barium oesophagrams. Atropine and sodium nitroprusside were studied in six of the BAC-treated and five controls using oesophageal manometry. Histologically several neuronal markers, B-NADPH-diaphorase and acetylcholine esterase histochemical staining were used. NADPH-diaphorase activity was assayed at the lower oesophageal sphincter (LOS) and 3 and 5 cm above LOS in both groups. Oesophagoscopy of the treated animals showed no mucosal inflammation, or strictures. Manometrically, LOS pressures were significantly higher in the BAC-treated group (25.7 +/- 8.6 mmHg) when compared to controls (8.7 +/- 1.8 mmHg). The oesophageal contraction amplitudes were similar in both groups. While sodium nitroprusside (SNP) significantly reduced the LOS pressure, atropine did not alter the resting LOS pressure in the BAC-treated animals. Histologically at the LOS the treated group showed: (i) absence of myenteric neurons, in contrast to prominent NADPH-diaphorase and other neuron and peptide markers in the control and (ii) increase in the number of nerve bundles that were not positive for AchE. No differences were seen in the oesophageal body between the groups. The NADPH-diaphorase assay showed a significant decrease of activity in the BAC-treated LOS, but no differences in the oesophageal body compared to controls. Several of these radiologic, manometric and histological observations resemble features of achalasia and the mechanism of the tonic pressure increase at this early time point appears to be due to a non-cholinergic mechanism.
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PMID:Evaluation of early events in the creation of amyenteric opossum model of achalasia. 895 39

Nasal vascular and secretory responses to local intra-arterial injection of acetylcholine (ACh) and vasoactive intestinal polypeptide (VIP) and to electrical stimulation of the nasal parasympathetic nerve fibres were recorded in dogs anaesthetized with pentobarbital. The influence of pretreatment with atropine and propranolol and the nitric oxide synthetase (NOS) inhibitor Nomega-nitro-L-arginine (L-NNA) was analysed. As a marker for NOS, NADPH-diaphorase (NADPH-d) histochemistry was studied in the sphenopalatine ganglion, trigeminal nerve and nasal mucosa. Local intra-arterial infusion of ACh and VIP evoked dose-dependent vasodilatation and nasal secretion which were not modified in the presence of L-NNA. The NO donor nitroprusside induced dose-dependent vasodilatation but no secretion. Atropine did not reduce the vasodilatation evoked by the parasympathetic nerve stimulation, but did reduce the secretory response by 55% (p < 0.05). During L-NNA infusion, the atropine-resistant vasodilatation evoked by parasympathetic nerve stimulation was reduced by a further 80% (p < 0.01) and the non-cholinergic secretory response was reduced by a further 30% (p < 0.05). Simultaneous infusion of the NO donor nitroprusside reversed the secretory response but not the vasodilator response to parasympathetic nerve stimulation. Histochemical studies revealed that NADPH-d activity was co-localized with VIP in parasympathetic axons. These observations suggest that NO could act as a non-cholinergic parasympathetic neurotransmitter in the vascular and secretory control of the dog nasal mucosa.
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PMID:Nitric oxide and parasympathetic vascular and secretory control of the dog nasal mucosa. 958 96

Nitric oxide (NO) is a major transmitter in mediating cerebral neurogenic vasodilation in several species. Recent findings have suggested that acetylcholine, which is costored with NO in cerebral perivascular nerves, plays a role in modulating NO release, presumably by acting on muscarinic (M) receptors on nitric oxidergic nerve terminals. The present study was designed using an in vitro tissue bath technique to pharmacologically characterize the presynaptic muscarinic-receptor subtype(s) that mediate modulation of NO release and therefore neurogenic vasodilation and to investigate further the possible mechanisms involved in this presynaptic modulation in porcine basilar arteries. Transmural nerve stimulation (TNS) elicited a frequency-dependent, tetrodotoxin-sensitive relaxation. The relaxation was abolished by nitro-L-arginine (30 microM) and was completely reversed by L-arginine and L-citrulline, but not by their D-enantiomers. Atropine (0.01-1 microM), pirenzepine (an M1-receptor antagonist, 0. 01-1 microM), and methoctramine (an M2-receptor antagonist, 0.01-1 microM), but not 4-DAMP (an M3-receptor antagonist) or tropicamide (an M4-receptor antagonist) at concentrations as high as 10 mM, significantly increased the TNS-elicited relaxation. This relaxation, on the other hand, was significantly attenuated by arecaidine but-2-ynyl ester tosylate (an M2-receptor agonist, 0.1 microM) but was not affected by McN-A-343 (an M1-receptor agonist, 1 microM). Double-labeling immunohistochemical study demonstrated that perivascular M2 receptor-immunoreactive fibers were completely coincident with NADPH diaphorase fibers. Furthermore, the muscarinic receptor-mediated modulation of TNS-elicited relaxation was completely prevented by omega-conotoxin GVIA (0.1 microM), a specific N-type Ca2+ channel inhibitor, but was still observed in the presence of tetraethylammonium (1 mM), 8-bromo-cAMP (0.5 mM), and pertussis toxin. It is concluded that the presynaptic M2 receptors on porcine cerebral perivascular nitric oxidergic nerves mediate inhibition of NO release. The inhibition is due primarily to a decreased Ca2+ influx through N-type Ca2+ channels.
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PMID:Mechanism of prejunctional muscarinic receptor-mediated inhibition of neurogenic vasodilation in cerebral arteries. 988 33