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)

Nitric oxide synthase(NOS) inhibitor,N omega-nitro-L-arginine methyl ester (L-NAME, 10-300 mg/kg) and L-NG-monomethyl-arginine (L-NMMA, 30-300 mg/kg) suppressed the swellings of adjuvant-injected paw of rats (25-54%) at day 2 and 8 when dosed intraperitoneally and orally for 4 days from day -1 to day 2 after adjuvant. L-NAME (30-300 mg/kg) also suppressed the edema of the non adjuvant-injected paws (15-42%) at day 28. Local injection of this inhibitor (2 and 10 mg/kg) was without effect. L-arginine (1 g/kg, i.p.), impaired the suppression by L-NAME. Bovine blood Cu, Zn-superoxide dismutase (SOD, 3 mg/kg, i.p.: 28% suppression) and L-NAME (30 mg/kg i.p.: 36% suppression) showed additive effect (52%) in adjuvant-injected paws at day 8 when co-injected. As the effect of 30 mg/kg L-NAME corresponded nearly to that of 10 mg/kg VoltarenR, this NOS inhibitor would be worth considering as an anti-inflammatory agent. Sodium nitroprusside (NO-donor) and methylene blue (guanylate cyclase inhibitor) had no effect. L-NAME was also suppressive when dosed after adjuvant inoculation and NO is involved in the development and maintenance of swelling.
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PMID:Nitric oxide and superoxide radical are involved in both initiation and development of adjuvant arthritis in rats. 816 99

The cavernous carotid artery, that portion of the internal carotid artery that lies within the intracranial cavernous sinus, is covered by arterial (luminal surface) and venous (external surface) endothelium. The reactivity of the isolated canine, cavernous carotid artery, precontracted with 10(-5) M 5-hydroxytryptamine, was studied by using in vitro perfusion and superfusion to evaluate the effects of vasoactive stimuli applied to the internal or external surface. Acetylcholine (10(-8)-10(-4) M), thrombin (0.01-1 U/ml) or calcium ionophore A23187 (10(-8) - 10(-6) M) on the luminal side produced concentration-dependent relaxations which were reduced by the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME, 10(-4) M) or by removing either the internal or both endothelia. Thrombin or ionophore A23187 on the external side produced concentration-dependent contractions which were reduced by removing either the external or both endothelia, and by meclofenamate (10(-5) M). Acetylcholine on the external side, produced a concentration-dependent contraction that was unaffected by meclofenamate or by removing the external or both endothelia. Sodium nitroprusside (10(-7) - 10(-5) M) induced similar relaxation on both sides and regardless of whether the arteries were with or without endothelium. These results suggest firstly, that the cavernous carotid artery responds to acetylcholine, thrombin or calcium ionophore A23187 by relaxing or contracting when these agents act on the luminal or the external surface respectively. Secondly, the arterial endothelium mediates relaxation to these three substances by releasing NO, whereas the venous endothelium mediates contraction to thrombin and ionophore A23187 by releasing a cyclooxygenase product.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reactivity of the dog cavernous carotid artery. The role of the arterial and venous endothelium. 830 86

It has become evident that complete elimination of the vasodilator response to agonists that require the release of nitric oxide (NO) is necessary for certain studies of the microcirculation. The A2 and A3 arterioles of the rat cremaster muscle microcirculation were studied by video-microscopy. At control, arterioles at rest or constricted by arginine vasopressin (AVP) were dilated by intra-arterially injected acetylcholine (ACh), intra-arterially injected adenosine (ADO) and topical adenosine. The NO antagonists, Nw-nitro-L-arginine methyl ester (L-NAME) and hydroquinone (HQ), which acts as an antagonist by generating free radicals, in maximal doses, individually partially blocked the vasodilator actions of intra-arterial ACh and intra-arterial ADO. Combining L-NAME and HQ eliminated the vasodilation by intra-arterial ACh and intra-arterial ADO. Sodium nitroprusside dilated the arterioles to the resting level or above at control and in the presence of the antagonists either individually or when combined. However, the NO antagonists did not block the arteriolar vasodilator responses to topical ADO. The reduction of the production of NO and enhancement of its destruction by superoxide radicals results in the total absence of the vasodilator response due to intra-arterially injected acetylcholine and adenosine. The data suggest that luminal ADO receptors cause arteriolar dilation by endothelial-dependent mechanisms and abluminal receptors cause dilation by another mechanism.
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PMID:Antagonism of acetylcholine and adenosine rat cremaster arteriolar vasodilation by combination of NO antagonists. 837 62

1. A study has been made of the modulation of high-voltage activated transient and sustained calcium currents in cultured neurones of avian ciliary ganglia by nitric oxide (NO) and arachidonic acid. 2. Sodium nitroprusside (100 microM) reduced the transient calcium current (ICa) on average by 31% and the sustained ICa by 32% during a test depolarization to +20 mV from a holding potential of -100 mV. This reduction was maintained for at least 30 min following a single application of sodium nitroprusside. 3. L-Arginine (270 microM) reduced the transient ICa on average by 28% and the sustained ICa by 22% and these effects were prevented by the presence of the NO-synthase competitive blocker NG-nitro-L-arginine methylester (L-NAME; 100 microM) in the bathing solution. 4. Arachidonic acid (50 microM) reduced the transient ICa on average by 28% and the sustained ICa by 33%. When added together, arachidonic acid (50 microM) and L-arginine (270 microM) produced the same effects as arachidonic acid alone. 5. Blocking the conversion of arachidonic acid to prostaglandins by addition of indomethacin (20 microM) to the bathing solution did not prevent the depression of either the transient or the sustained calcium current during application of arachidonic acid (50 microM). The effects of arachidonic acid were also not occluded by L-NAME (100 microM) when present in the bathing solution. 6. Inhibiting the biosynthesis of leukotrienes by applying L-663,536 (MK-886; 3 microM) to the bathing solution prevented the depression of both components of ICa during application of arachidonic acid (50 microM). 7. These results indicate that endogenous NO and arachidonic acid pathways are present in parasympathetic ciliary neurones, and that both act to depress high-voltage, gated, calcium channel activity.
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PMID:Nitric oxide and arachidonic acid modulation of calcium currents in postganglionic neurones of avian cultured ciliary ganglia. 839 90

The present study was designed to investigate whether in vivo and in vitro erythropoietin (EPO) production is modulated by nitric oxide (NO) and cyclic guanosine 3',5'-monophosphate (cGMP). Serum levels of EPO in ex-hypoxic polycythemic mice were significantly increased after injections of 200 micrograms/kg sodium nitroprusside for 4 d. One injection of NG-nitro-L-arginine methyl ester (L-NAME) produced a significant dose-related decrease in serum levels of EPO in ex-hypoxic polycythemic mice in response to hypoxia. When EPO producing Hep3B cells were incubated in 1% O2 for 30 min, cGMP levels in the Hep3B cells were significantly elevated, compared with cells incubated in 20% O2. The elevation of cGMP by hypoxia was inhibited by L-NAME (100 microM). Sodium nitroprusside (10 and 100 microM) and NO (2 microM) also significantly increased cGMP levels in Hep3B cells. L-NAME, LY 83583 (6-Anilino-5,8-quinolinedione, a soluble guanylate cyclase inhibitor), and Rp-8-Bromo-cGMPS (Rp-8-Bromo-guanosine 3',5'-cyclic monophosphothioate, a cGMP-dependent protein kinase inhibitor) significantly inhibited the hypoxia-induced increase in medium levels of EPO in Hep3B cells. 8-Bromo-cGMPS produced a dose-dependent decrease in EPO messenger RNA levels in Hep3B cells in response to hypoxia. 8-Bromo-cGMP (10(-3) M) produced significant increases in medium levels of EPO in Hep3B cell cultures incubated under normoxic conditions, which was enhanced by the phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine (0.2 mM). These results suggest that NO and cGMP may interact in modulating hypoxic stimulation of EPO production.
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PMID:Interaction of nitric oxide and cyclic guanosine 3',5'-monophosphate in erythropoietin production. 839 29

1. The role of the endothelium in the effects of cooling on the response to cholinoceptor stimulation of the rabbit central ear (cutaneous) and femoral (non-cutaneous) arteries was studied using 2 mm long cylindrical segments. 2. Concentration-response curves for acetylcholine (10(-9)-10(-5) M), methacholine (10(-9)-10(-5) M) and sodium nitroprusside (10(-9)-10(-4) M) were isometrically recorded in arteries under conditions, with and without endothelium or following pretreatment with the nitric oxide-synthesis inhibitor NG-nitro-L-arginine methyl ester (L-NAME, 10(-6)-3 x 10(-4) M) at 37 degrees C and at 24 degrees C (cooling). 3. Ear and femoral arteries showed endothelium-dependent relaxation to acetylcholine and methacholine at 37 degrees C and 24 degrees C. The extent of relaxation of the control ear arteries, but not of the control femoral arteries, to acetylcholine and methacholine increased during cooling. 4. L-NAME (10(-6)-3 x 10(-4) M) reduced in a concentration-dependent way the response of ear arteries to acetylcholine at both 37 degrees C and 24 degrees C, this reduction being more potent at 37 degrees C. L-Arginine (10(-5)-10(-3) M) reversed in a concentration-dependent manner the inhibitor effects of 10(-5) M L-NAME at both temperatures. 5. Sodium nitroprusside caused a concentration-dependent relaxation in both arteries that was endothelium-independent. However, the extent of relaxation to this nitrovasodilator in ear and femoral arteries was lower at 24 degrees C. 6. These results suggest that cooling augments the reactivity of cutaneous (ear) arteries, but not that of non-cutaneous (femoral) arteries to cholinoceptor stimulation by endothelium-mediated mechanisms.Cooling could therefore facilitate the stimulated release of endothelial nitric oxide in cutaneous vessels.
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PMID:Role of the endothelium in the response to cholinoceptor stimulation of rabbit ear and femoral arteries during cooling. 849 47

This study examines the role of nitric oxide (NO) in the regulation of calcium absorption in the small intestine. Calcium absorption was quantified by measuring 45Ca++ transport from lumen to blood in an intestinal segment (duodenum and 20 cm of the proximal jejunum) perfused by both intraluminal and vascular routes in anesthetized rats. When administered i.v. as bolus injections, NG-nitro-L-arginine methyl ester (L-NAME, 10 mg.kg-1), an inhibitor of NO biosynthesis, decreased calcium absorption with a concomitant increase in blood pressure and a decrease in mesenteric blood flow. Conversely, the nitrovasodilators 3-morpholinosydnonimine (2 mg.kg-1) and S-nitroso-N-acetylpenicillamine (10 micrograms.kg-1), which generate NO spontaneously, both increased calcium absorption with no change in mesenteric blood flow. When infused i.v., L-NAME (3 mg.hr-1.kg-1 for 40 min) induced a decrease in calcium absorption that was reversed by the NO donor sodium nitroprusside (1.5 mg.hr-1.kg-1 when infused for the last 20 min of the 40-min L-NAME infusion). Sodium nitroprusside infusion (1.5 mg.hr-1.kg-1) caused an increase in calcium absorption that was not reversed by L-NAME (3 and 30 mg.hr-1.kg-1). The present findings suggest that NO is involved in basal calcium absorption in rat small intestine in vivo.
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PMID:Intestinal absorption of calcium in vivo is dependent on endogenous nitric oxide. 853 Nov 12

We have evaluated the role of nitric oxide (NO) on the cyclooxygenase pathway in mouse glial cells. Exposure of primary cultures of neonatal mouse cortical astrocytes to bacterial lipopolysaccharide (LPS; 1 microgram/ml, 18 h) caused an increase in the release of both nitrite (NO2-) and prostaglandin E2 (PGE2), products of NO synthase (NOS) and cyclooxygenase, respectively. Production of both, NO2- and PGE2 by astrocytes, was inhibited by the exposure of the NOS inhibitor Nw-nitro-L-arginine methyl ester (L-NAME: 1, 10, and 100 microM) in a dose related manner. Besides, other NOS inhibitors such as Nitro L-arginine (NNA: 10(-3) M) prevented the increase in PGE2 release from LPS-stimulated astrocytes. Sodium nitroprusside (SNP; 100-200 microM) used as a NO donor caused a dose-related enhancement in the accumulation of PGE2 induced by LPS and the presence of hemoglobin blocked the SNP effects. The exposure to SNP counteracted the decrease of PGE2 production in LPS-treated astrocytes in which NO synthesis was blocked by L-NAME. In addition, SNP also enhanced the synthesis of PGE2 following exogenous arachidonic acid astrocytes exposure. Interestingly, this effect was blocked by indomethacin. Treatment of astrocytes cultures with dexamethasone (0.1, 1 microM) blocked dose-relatedly the LPS-induced release of both NO2- and PGE2. As expected, the presence of indomethacin (1, 10, and 20 microM) prevented in a dose related fashion, PGE2 production by astrocytes following exposure to LPS. These results strongly indicate that in astroglial cells, NO is able to activate the cyclooxygenase pathway.
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PMID:Evidence for cyclooxygenase activation by nitric oxide in astrocytes. 856 68

1. The contribution of nitric oxide (NO) and vasoactive intestinal polypeptide (VIP) to non-adrenergic non-cholinergic (NANC) relaxations in the pig gastric fundus was investigated. 2. Circular and longitudinal muscle strips were mounted for isotonic registration in the presence of atropine and guanethidine; tone was raised with 5-hydroxytryptamine. Electrical field stimulation with 10 s trains at 5 min intervals induced responses were abolished by tetrodotoxin. 3. The short-lasting as well as the sustained electrically induced NANC relaxations were significantly reduced by NG-nitro-L-arginine methyl ester (L-NAME). Pretreatment with L-arginine but not D-arginine, prevented the inhibitory effect of L-NAME except for sustained relaxations in the longitudinal muscle strips. 4. Sodium nitroprusside, forskolin, zaprinast and 3-isobutyl-l-methylxanthine induced concentration-dependent relaxations. Exogenous NO mimicked the short-lasting electrically induced relaxations, while endogenous VIP evoked sustained relaxations. The responses to exogenous NO and VIP were not influenced by tetrodotoxin and L-NAME. 5. alpha-Chymotrypsin abolished the responses to exogenous VIP but only moderately reduced NANC relaxations induced by continuous electrical stimulation. Zaprinast potentiated the relaxant responses to sodium nitroprusside and increased the duration of the NANC relaxations induced by electrical stimulation with 10 s trains in circular muscle strips but not in longitudinal muscle strips. 6. The cyclic GMP and cyclic AMP response to electrical stimulation, NO and VIP was measured in circular muscle strips. Short-lasting as well as sustained electrical field stimulation induced an approximately 1.5 fold increase in cyclic GMP content, while NO induced nearly a 40 fold increase. An increase in cyclic AMP content was obtained only with sustained electrical field stimulation. 7. Immunocytochemistry for NO synthase (NOS) revealed immunoreactive neuronal cell bodies in the submucous and myenteric plexuses and nerve fibres in both the circular and longitudinal muscle layer; double-labelling for NOS and VIP showed that VIP coexists in a major part of the intrinsic neurones. NADPH diaphorase-histochemistry showed the same pattern of nitrergic neurones and nerves as NOS-immunocytochemistry. 8. It is concluded that a cyclic GMP- and a cyclic AMP-dependent pathway for relaxation is present in both the circular and longitudinal muscle layer of the pig gastric fundus. NO appears to contribute to short-lasting as well as sustained NANC relaxations. A peptide, possibly VIP, may be involved during sustained stimulation at lower frequencies of stimulation.
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PMID:Study of NO and VIP as non-adrenergic non-cholinergic neurotransmitters in the pig gastric fundus. 864 Mar 40

The role of nitric oxide (NO) as well as its interaction with prostaglandins (PG) in setting the limits of autoregulation of retinal blood flow (RBF) and choroidal blood flow (ChBF) were studied in newborn pigs (1-5 d old). Blood flows were measured by the microsphere technique. Low and high ocular perfusion pressures (OPP) were induced by inflating balloon-tipped catheters placed at the aortic root and isthmus, respectively. Animals were treated with the NO synthase inhibitors, NG-nitro-L-arginine methyl ester (L-NAME, 1 mg/kg followed by 50 mu g/kg/min; n = 12) or NG-monomethyl-L-arginine (L-NMMA, same dose as L-NAME; n = 3), or with saline (n = 12). In separate animals (n = 42), guanosine 3',5'-cyclic monophosphate (cGMP), the second messenger for NO, and PG were measured at an average OPP of 90 mm Hg and 125 +/- 6 mm Hg; cGMP levels served as an index of NO release. The effect of the NO donor sodium nitroprusside on choroidal vessel diameter was determined using video imaging of isolated eyecup preparations. In control animals RBF was constant only within a range of 30 to 80 mm Hg OPP (r = 0.03, p > 0.9). There was no autoregulation of ChBF which increased as a function of OPP (tau = 0.58-0.72, p < 0.01). L-NAME and L-NMMA prevented a change in RBF and ChBF from 30 to 146 mm Hg [the highest OPP studied (r < 0.3, p > 0.15)] and caused an increase in retinal as well as choroidal vascular resistance as OPP was raised; these agents did not affect ocular blood flow at OPP < 30 mm Hg. Elevated OPP caused increases in cGMP, 6-keto-PGF1alpha, and PGE2 in the choroid (a vascular tissue), which were prevented by L-NAME and L-NMMA. Sodium nitroprusside caused a dilatation of choroidal vessels in isolated eyecup preparations, which was significantly attenuated by indomethacin. Data suggest a role for NO in the autoregulation of RBF and ChBF in the newborn such that a release of NO during a rise in OPP prevents adequate constriction necessary for maintaining RBF and ChBF constant; data also suggest that the vasodilator effect of NO might in part be mediated through a release of PG.
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PMID:Nitric oxide in retinal and choroidal blood flow autoregulation in newborn pigs: interactions with prostaglandins. 892 70

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