UMLS:C0406810 - FACTA Search

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Query: UMLS:C0406810 (NAME)
13,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Organ Weight, hematologic and blood chemistry values were determined to establish reference values in the female ferret. Organ weight per kg body weight was calculated for various organs. Body surface area (BSA) was also determined by the direct method, and K values (constant) were calculated. The K value was 3.48 in the Dubois and Dubois equation, and 9.69 in the Meeh-Rubner equation. Blood samples were used to record 10 hematologic and 57 serum (plasma) chemistry values, and 7 immunological parameters. Among hematologic values, values whose coefficient of variation (cv) exceeded 30% were RBC, WBC and PLT. In blood chemistry, the CV of gamma-G, UA, ZTT, GPT, gamma-GTP, MAO, ALD and IgG exceeded 30%. In the total amino acid analysis, only the CV of TAU exceeded 30%. Electrophoretograms of amylase and CPK isozyme were quite different from those of humans. Although 1-MEHIS, 3-MEHIS and CAR have not been detected or are present in trace amounts in human plasma, concrete values were detected in female ferret plasma. Hematologic and serum chemistry values were in general agreement with normal values seen in cats and dogs. However, the alpha 1-G percentage, and ALP and amylase activities were lower than the corresponding values in cats and dogs. The RBC count, RET-C percentage and LDH activities were higher than in cats and dogs. Since there have been no comprehensive articles on reference values for the female ferret, the present report contributes to studies that involve this animal as an experimental model.
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PMID:Reference values for organ weight, hematology and serum chemistry in the female ferret (Mustela putrius furo). 851 87

Nitric oxide (NO) production reportedly regulates guanosine 3', 5'-cyclic monophosphate (cGMP) formation and Ca2+ influx in pancreatic acini. We have investigated the functional roles of the NO/cGMP messenger system in rat pancreatic acini. In dispersed acini, the levels of amylase secretion, cytosolic [Ca2+]([Ca2+]i), NO synthase, and cGMP were measured. The NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME, 0.01-100 microM) had no effect on amylase secretion induced by various concentrations of carbachol, cholecystokinin octapeptide (CCK-8) or the high affinity CCK agonist, JMV-180. Similarly, L-NAME up to 100 microM did not affect the changes in Ca2+ spiking evoked by these secretagogues; nor was Ca2+ entry, refilling or oscillation altered by L-NAME. Sub- and supramaximal concentrations of these secretagogues did not change NO synthase activities compared with basal levels. While sodium nitroprusside (SNP), a NO donor, caused a 9.4-fold increase in cGMP levels compared with basal levels, carbachol, CCK-8 and JMV-180 had no effect. In addition, the guanylate cyclase inhibitor LY 83583 (10 nM to 10 microM) altered neither amylase secretion nor Ca2+ signaling induced by these secretagogues. These findings indicate that the stimulatory action of carbachol or CCK-8 is not mediated by NO or cGMP. To investigate whether cGMP stimulates pancreatic secretion we showed that both SNP and a cell-permeant cGMP analog at 0.1-1 mM stimulated amylase secretion and Ca2+ transients to a level equal to 10-15% and 13-24%, respectively, of those observed with maximal concentrations of secretagogues. The guanylate cyclase activator guanylin (1-10 microM), which increased cGMP levels 2.4-fold compared with basal levels, elicited a small amount of amylase secretion and a small Ca2+ transient. In conclusion, exogenous NO is capable of increasing endogenous cGMP, which results in a modest increase in the [Ca2+]i transient and pancreatic amylase secretion. However, the NO/cGMP system does not appear to be involved significantly in the mediation of Ca2+ signaling and amylase secretion stimulated by carbachol and CCK-8.
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PMID:Effect of uncoupling NO/cGMP pathways on carbachol- and CCK-stimulated Ca2+ entry and amylase secretion from the rat pancreas. 909 53

The effects of cadmium, l-arginine (nitric oxide precursor) and N(omega)-nitro-l-arginine methyl ester (l -NAME) as a nitric oxide synthesis inhibitor and cotreatment of them on rat submandibular secretory function were studied. Pure submandibular saliva was collected intraorally by micro polyethylene cannula from anaesthetized rats using pilocarpine as secretagogue. Fourteen days treatment with 10 mg l(-1)cadmium as cadmium chloride in drinking water caused significant alterations on salivary function. Salivary flow rate, total protein concentration and amylase activity of saliva were decreased while secretion of calcium was increased by cadmium. Two weeks treatment of rats with l -arginine (2.25%) in drinking water caused an increase in submandibular gland weight. Flow rate was reduced by l-NAME. The total protein concentration of saliva was increased by l-arginine while decreased by l-NAME. Calcium concentration of saliva was reduced by l-arginine and increased by l-NAME. Cotreatment of cadmium with l-arginine prevented cadmium-induced reduction of flow rate while l-NAME cotreatment potentiated cadmium-induced reduction of flow rate. l-arginine showed a preventive effect on cadmium-induced decrease of protein concentration and reached control levels. l-arginine potentiated cadmium-induced increase of saliva calcium concentration. It is confirmed that nitric oxide (NO) has a role in salivary gland function. It is also concluded that cadmium inhibitory effects on salivary gland function are modulated by the NO system as it is observed that the cadmium inhibitory effect on submandibular gland function is diminished by l-arginine and extended by l-NAME. Considering the properties of cadmium substitution for calcium in many intracellular events, different types of alterations can be discussed.
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PMID:Alteration by cadmium of rat submandibular gland secretory function and the role of the l-arginine/nitric oxide pathway. 1105 13

The effects of lead acetate, L-arginine (nitric oxide precursor) and L-NAME (nitric oxide synthesis inhibitor) on rat submandibular secretory function were studied. Pure submandibular saliva was collected intraorally from anaesthetized rats by a micro polyethylene cannula using pilocarpine as secretagogue. Treatment for twenty-eight days with three doses of lead acetate (0.01%, 0.04%, 0.05% w/v) in drinking water caused significant alterations on salivary function. Salivary flow rate was decreased by lead at all doses used. The total protein concentration and amylase activity of saliva were both decreased by lead (0.04% and 0.05%). All doses of lead decreased saliva calcium concentrations. Two weeks' treatment of rats by L-arginine (2.25% w/v) and L-NAME (0.7% w/v) in drinking water also affected the saliva secretory function. L-Arginine caused increase in submandibular gland weight. The saliva flow rate was reduced by L-NAME. The total protein concentration of saliva was increased by L-arginine and decreased by L-NAME. Amylase activity was reduced by L-arginine treatment. Calcium concentration was reduced by L-arginine and increased by L-NAME. Concurrent L-arginine treatment with lead acetate recovered lead-induced reduction of flow rate but L-NAME potentiated it. Concurrent therapy of lead and L-NAME resulted in greater reduction of protein concentration when compared to that of lead. L-Arginine showed a preventive effect on lead-induced decrease of protein concentration. Both L-arginine and L-NAME prevented lead-induced reduction in calcium concentration. It is concluded that nitric oxide plays a role in salivary gland function. Also lead acetate inhibitory effect on submandibular function is somewhat diminished by L-arginine and partially increased by L-NAME. It seems that lead acetate interacts with nitric oxide modulatory role in salivary gland.
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PMID:L-arginine/nitric oxide pathway and interaction with lead acetate on rat submandibular gland function. 1112 98

Methacholine (MCh) interacted with M(3) muscarinic receptors in rat parotid tissue slices and induced amylase secretion. MCh- and calcimycin-induced exocytosis was completely inhibited by N-[2-(N-(4-chlorocinnamyl)-N-methylaminomethyl)phenyl]-N-[2-hydroxyethyl]-4-methoxybenzenesulfonamide, N(G)-nitro-L-arginine methylester (L-NAME), 1H-(1,2,4)-oxadiazolo[4,3-a]quinoxaline-1-one, and 2-(4-carboxyphenyl)-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide, suggesting that activations of calmodulin (CaM) kinase II, nitric oxide synthase (NOS), and cGMP-dependent protein kinase (PKG) were coupled with the exocytosis. These suggestions were supported by the results that exposure of the slices to MCh induced a rapid increase in these enzyme activities. Western blot analysis showed that neuronal NOS (nNOS) was expressed in isolated parotid acinar cells of rats. To measure nitric oxide (NO) production in response to the stimulation with MCh in real time, the isolated parotid acinar cells had been preloaded with 4,5-diaminofluorescein diacetate and incubated with the agonist. MCh (1 microM) induced a fast increase in 4,5-diaminofluorescein fluorescence, corresponding to an increase in the NO synthesis in the presence of extracellular Ca(2+) but not in the absence of it. When the isolated parotid acinar cells preloaded with L-NAME or 2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetrakis (acetoxymethylester) were treated simultaneously with MCh, the increase in the fluorescence also was not observed. The MCh-induced increase in the fluorescence was not observed in the cells incubated in the absence of extracellular calcium, showing the importance of Ca(2+) entry from extracellular sites for MCh-induced NOS activation. These results indicate that nNOS is endogenously present in rat parotid acinar cells and that the rapid activation of this enzyme together with those of CaM kinase II and PKG contributes to MCh-induced amylase secretion.
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PMID:Activation of endogenous nitric oxide synthase coupled with methacholine-induced exocytosis in rat parotid acinar cells. 1190 93

Muscarinic receptors play an important role in secretory and vasodilator responses in rat salivary glands. Nitric oxide synthase (NOS) activity was found coupled to muscarinic receptor activation as well as to nitric oxide-mediated amylase secretion elicited by carbachol. Parotid glands presented a predominant M(3) and a minor muscarinic M(1) acetylcholine receptor population, though carbachol stimulated NOS activity only through muscarinic M(3) receptors as revealed in the presence of 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP) and pirenzepine. Amylase secretion induced by carbachol appeared to be partly mediated by nitric oxide and nitric oxide-induced signaling since N-nitro-L-arginine methyl ester (L-NAME) inhibited the effect as well as did methylene blue. A negative regulation of NOS by protein kinase C activation in the presence of a high concentration of carbachol was seen in parotid glands and this inhibition was paralleled by amylase secretion.
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PMID:Activation of nitric oxide synthase through muscarinic receptors in rat parotid gland. 1193 89

Protease-activated receptor-2, a G protein-coupled receptor activated by serine proteases such as trypsin, tryptase and coagulation factors VIIa and Xa, modulates pancreatic and salivary exocrine secretion. In the present study, we examined the distribution of PAR-2 in the pancreas and parotid gland, and characterized the PAR-2-mediated secretion of amylase by these tissues in vivo. Immunohistochemical analyses using the polyclonal antibody against rat PAR-2 clearly showed abundant expression of PAR-2 in rat pancreatic and parotid acini. The PAR-2 agonist SLIGRL-NH2, administered intraperitoneally (i.p.) at 1-10 micromol/kg and 1.5-15 micromol/kg, in combination with amastatin, an aminopeptidase inhibitor, facilitated in vivo secretion of pancreatic and salivary amylase in a dose-dependent manner, respectively, in the mouse. The PAR-2-mediated secretion of pancreatic amylase was abolished by pretreatment with N(G)-nitro-L-arginine methyl ester (L-NAME), an NO synthase inhibitor. The secretion of salivary amylase in response to the PAR-2 agonist at a large dose, 15 micromol/kg, but not at a smaller dose, 5 micromol/kg, was partially reduced by L-NAME. Pretreatment with capsaicin for ablation of the sensory neurons did not modify the PAR-2-mediated secretion of pancreatic and salivary amylase in the mouse. In conclusion, our study demonstrates expression of PAR-2 in rat pancreatic acini as well as parotid acini and indicates that nitric oxide participates in the PAR-2-mediated in vivo secretion of pancreatic amylase, and, to a certain extent, of salivary amylase, although capsaicin-sensitive sensory neurons, known to be activated by PAR-2, are not involved in the evoked pancreatic or salivary amylase secretion.
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PMID:Protease-activated receptor-2 (PAR-2) in the pancreas and parotid gland: Immunolocalization and involvement of nitric oxide in the evoked amylase secretion. 1223 4

Nitric oxide (NO) is a short-lived free radical and is a widespread intra- and intercellular messenger molecule involved in various physiological functions. We have demonstrated previously that the muscarinic agonist methacholine induces endogenous generation of NO in rabbit parotid acinar cells. Since methacholine also simultaneously evokes amylase secretion, we investigated the effect of NO on the methacholine-induced exocytotic amylase secretion in rabbit parotid acinar cells. Methacholine-evoked amylase secretion was clearly reduced in the absence of extracellular Ca(2+). The Ca(2+)-mobilizing reagents A23187 and thapsigargin, which stimulate NO generation, also evoked amylase secretion. This response seemed to be caused by NO generated by the activation of endogenous Ca(2+)-regulated NO synthase. However, N(G)-nitro-L-arginine methyl ester (L-NAME), a specific NOS inhibitor, and the NO scavenger haemoglobin had no effect on methacholine-induced amylase secretion. The NO generator sodium nitroprusside (SNP) failed to evoke amylase release. We further studied the effects of L-NAME and SNP on methacholine-induced amylase secretion in crudely dispersed parotid gland cell clusters containing nerve tissue. In this preparation, L-NAME inhibited methacholine-induced amylase secretion and SNP evoked amylase secretion. It is thus unlikely that NO contributes directly to methacholine-induced amylase secretion in rabbit parotid acinar cells. NO appears rather to affect to nerve tissues in the cell suspension.
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PMID:Evidence that nitric oxide does not directly contribute to methacholine-induced amylase secretion in rabbit parotid acinar cells. 1268

An enhanced formation of nitric oxide (NO), due to the induction of inducible nitric oxide synthase (iNOS), has been implicated in the pathogenesis of shock and inflammation, but its role in acute pancreatitis still remains controversial. To clarify the role of NO in acute pancreatitis, the present experiment investigated the expression of iNOS and the effect of NOS inhibition on cerulein-induced pancreatitis in rats. Group I received intraperitoneal (ip) injection of normal saline. Group II received two ip injections of cerulein (20 microgram/kg). Group III received injections of N(G)-nitro-L-arginine methyl ester (L-NAME) (30 mg/kg) with cerulein. Group IV received L-arginine (250 mg/kg) with cerulein and L-NAME. The expression of iNOS in the pancreas was examined by western blot analysis. The plasma concentration of NO metabolites was measured. The severity of pancreatitis was assessed by measuring serum amylase, pancreas water content and histopathological examination. Compared with controls, the cerulein group displayed significantly increased expression of iNOS and raised plasma NO metabolites. Treatment with L-NAME significantly decreased hyperamylasemia, plasma NO level, and the extent of pancreatic injury. Treatment with L-arginine reversed the effects of L-NAME. These findings suggest that an enhanced formation of NO by iNOS plays an important role in the development of acute pancreatitis, and inhibition of NO production has the beneficial effects in reducing pancreas injury.
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PMID:The role of nitric oxide in experimental cerulein induced pancreatitis. 1292 28

Central neuropeptides play a role in many physiological functions through the autonomic nervous system. We have recently demonstrated that central injection of a thyrotropin-releasing hormone (TRH) analog increases pancreatic blood flow through vagal and nitric oxide-dependent pathways. In this study, the central effect of a TRH analog on experimental acute pancreatitis was investigated in rats. Acute pancreatitis was induced by two intraperitoneal injections of cerulein (40 microg/kg) at 1-h interval. Either stable TRH analog, RX 77368 (5-100 ng), or saline was injected intracisternally 15 min before the first cerulein injection under ether anesthesia. Serum amylase level was measured before and 5 h after the first cerulein injection. Pancreatic wet/dry weight ratio and histological changes were also evaluated. Intracisternal TRH analog inhibited cerulean-induced elevation of serum amylase level, increase in pancreatic wet/dry weight ratio and pancreatic histological changes, such as interstitial edema, inflammation and vacuolization. The pancreatic cytoprotection induced by central TRH analog was abolished by subdiaphragmatic vagotomy and N(G)-nitro-L-arginine-methyl ester (L-NAME), but not by 6-hydroxydopamine (6-OHDA). Intravenous administration of the TRH analog did not influence cerulein-induced acute pancreatitis. These results indicate that the TRH analog acts in the central nervous system to protect against acute pancreatitis through vagal and nitric oxide-dependent pathways.
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PMID:Protective effect of central thyrotropin-releasing hormone analog on cerulein-induced acute pancreatitis in rats. 1558 22

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