Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.6.5.2 (NQO1)
 6,196 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the present study was to analyze the neurochemical properties of the centrifugal visual system (CVS) of the quail using an immunohistochemical approach by testing 16 neuropeptides (angiotensin: ANG, bradykinin: BK, cholecystokinin, dynorphin, L and M-enkephalin, beta-endorphin: beta-END, galanin, alpha-neoendorphin, neurokinin A, neuropeptide Y (NPY), ocytocin, somatostatin, substance P, vasopressin, vasoactive intestinal polypeptide) and three neurotransmitters or their synthetic enzymes (choline acetyltransferase: ChAT, tyrosine hydroxylase: TH, serotonin: 5-HT and nitric oxide synthase: NOS, including the histochemical nicotinamide adenine dinucleotide phosphate diaphorase technique). For each substance, the somatic and afferent fiber and terminal labeling was analyzed within the nucleus isthmo-opticus (NIO) and the ectopic area (EA) and compared with that of retinopetal cell bodies labeled retrogradely with RITC following its intraocular injection (double-labeling procedure). The results showed that none of the centrifugal neurons were reactive to any of the substances tested. In contrast, all with the exception of ANG, BK and beta-END, labeled fibers and terminals within the EA and only four (ChAT, 5-HT, NPY and NOS) within the NIO. Possible sources of these immunoreactive fibers terminating in the NIO and EA were investigated by mapping the somatic immunolabeling of the different substances within brainstem regions previously shown by Miceli and other authors to project upon the centrifugal neurons. The data suggests that, besides the rapid retino-tecto-NIO-retinal loop, which facilitates the transfer of meaningful or more relevant information within particular portions of the visual field, the multiple afferent input which stems from various brainstem regions utilizes a wide range of neuroactive substances. Some of these afferent projections upon the centrifugal neurons appear to belong to nonspecific systems which might play a role in modulating the excitability of centrifugal neurons as a function of arousal.
 ...
PMID:An immunohistochemical study of putative neuromodulators and transmitters in the centrifugal visual system of the quail (Coturnix japonica). 971 61

This study examined the occurrence of endothelial nitric oxide (NO)-synthase (NOS-III) in terminal mesenteric vessels and the involvement of NO in microvascular permeability. Possible effects were studied in bradykinin (BK)-induced and basal conditions. NOS expression was investigated by using NOS-III immunohistochemistry and nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase histochemistry on the light- and electron-microscopic levels. Permeability was examined in dissected mesenteries of male rats weighing 250-300 g. Tissue treatment was performed with BK (100 nM), sodium nitroprusside (SNP, 1 and 10 microM), L-nitroarginine (L-NA, 300 microM), BK and L-NA, BK and SNP, L-NA and SNP, as well as with BK, SNP (10 microM), and the guanylylcyclase inhibitor ODQ (10 microM), and BK and ODQ alone. Pharmacologically induced permeability changes were studied with fluorescein isothiocyanate (FITC)-dextran 70 kDa as a tracer for macromolecular transport. Video images were analyzed with computer determination of integrated optical density (IOI). Results were statistically verified by analysis of variance and t test. Microvascular permeability was increased by 168% after BK treatment and was enhanced by NO-synthesis inhibition with L-NA by 607%. However, the NO donor SNP led to a reduced tracer extravasation to 105 and 58%, respectively, an effect blocked by ODQ. Under basal conditions without prior BK induction, L-NA also causes an increase of IOI by 25%, whereas coapplication with SNP resulted in only a 10% increase of permeability. These results point out that NO has a modulatory role for microvascular permeability by supporting the barrier function of the endothelial lining in stimulated and nonstimulated conditions.
 ...
PMID:Nitric oxide decreases microvascular permeability in bradykinin stimulated and nonstimulated conditions. 1036 98

Our previous studies have shown that selective inhibition of nitric oxide in the brain reduces pressor responses to activation of cardiac sympathetic afferents, thus suggesting that nitric oxide is involved in central regulation of cardiac-cardiovascular sympathoexcitatory reflexes. Central neural regions in which nitric oxide-producing neurons are activated during these reflexes have not been well characterized. In the present study, we located nitric oxide-producing neurons in the brain stem activated by the input from cardiac sympathetic afferents by detecting colocalization of c-Fos immunoreactivity with nitric oxide synthesizing neurons. Expression of c-Fos has been used as a marker of activated neurons. Nitric oxide-producing neurons were identified by histochemical labeling of nicotine adenine dinucleotide phosphate-diaphorase (NADPH-d). In anesthetized cats with bilateral barodenervation and cervical vagotomy, bradykinin (1-10 microg in 0.1 ml; n=6) was applied to the anterior surface of the left ventricle six times every 20 minutes. Repetitive application of bradykinin consistently increased blood pressure, while the vehicle for bradykinin (0.9% saline, n=5) produced no responses. A substantial fraction (6-27%) of NADPH-d positive neurons displayed Fos immunoreactivity in the nucleus of the solitary tract, caudal and rostral ventral lateral medulla, lateral tegmental field, locus coeruleus and parabrachial nucleus in the bradykinin-treated cats. However, either no or rare (1-4%) double-labeled cells were found in these regions in control animals. Thus, nitric oxide-producing neurons are activated in several regions in the brain stem during stimulation of cardiac sympathetic afferents by bradykinin. Our data suggest that nitric oxide functions as a neurotransmitter/modulator in these areas to regulate the cardiac sympathoexcitatory reflexes.
 ...
PMID:Activation of nitric oxide-producing neurons in the brain stem during cardiac sympathoexcitatory reflexes in the cat. 1253 50