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)

The roles of VIP and NO in vagally mediated relaxations of the gastric corpus were investigated in the anaesthetized ferret. Intracorpus pressure was recorded manometrically during electrical stimulation of the cervical vagus nerve in three groups of animals: one control group (n = 6), one group treated with an inhibitor of NO synthesis (NG-nitro-L-arginine methyl ester (L-NAME), 1.6 mg/kg); and a third group which had been immunized, prior to the experiment, with a VIP-thyroglobulin conjugate (25 nmol equivalent) in Freund's complete adjuvant. In control animals, following treatment with atropine (100 micrograms/kg), vagal stimulation resulted in a frequency dependent fall in intracorpus pressure with the maximum response at 5 Hz of 2.2 +/- 0.3 cm H2O. Two components of the response could be observed: an initial rapid fall over the first 10 s of stimulation followed by a slower decline over the remainder of the stimulation period. In animals treated with L-NAME (n = 6) the initial rapid response was significantly reduced at all frequencies of stimulation (P < 0.05 - P < 0.005, Mann-Whitney U-test) leaving only the slower second component. In immunized animals (n = 6) the initial rapid response to vagal stimulation was not different from control but the slower second component was significantly reduced at 1 Hz (P < 0.005). We conclude that the response to vagal stimulation appears to consist of two components which can be differentiated using L-NAME and autoimmunization to VIP.
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PMID:Role of nitric oxide and vasoactive intestinal polypeptide in vagally mediated relaxation of the gastric corpus in the anaesthetized ferret. 836 53

In eight anesthetized New Zealand White rabbits, the aorta was cannulated in situ for measurement of hydraulic conductance (Lp) at different pressures with and without endothelium. De-endothelialization increased Lp at > or = 75 mmHg but not at 50 mmHg. Because endothelium resists transmural water flow, the endothelium must also increase medial Lp at 50 mmHg. To determine whether this effect results from secretion of endothelial-derived relaxing factor (EDRF), Lp was measured in eight rabbits in the presence and absence of NG-nitro-L-arginine methyl ester (L-NAME), an inhibitor of EDRF synthesis. At 50 mmHg L-NAME reduced Lp from 6.79 +/- 2.19 to 2.59 +/- 1.41 (SD) x 10(-8) (P < 0.05, paired Student's t test). After L-NAME was removed, Lp returned to its control value. At 125 mmHg L-NAME did not significantly change Lp, although endothelial permeability seemed to increase. L-NAME did not affect Lp of nine de-endothelialized vessels at either pressure. An additional five experiments showed that the effect of L-NAME at 50 mmHg was reversed by L-arginine. Eleven additional experiments demonstrated that NG-nitro-D-arginine methyl ester does not affect Lp at 50 mmHg. These results indicate that EDRF increases Lp of the rabbit aorta at low pressures.
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PMID:Endothelium increases medial hydraulic conductance of aorta, possibly by release of EDRF. 843 Aug 54

The effects of i.p. administration of the nitric oxide synthase inhibitor NG-nitro-L-arginine methylester (L-NAME) and its inactive isomer, D-NAME, were tested in two nociceptive paradigms in the rat. In the first paradigm, rats were lightly anaesthetized with a mixture of chloral hydrate (120 mg/kg, i.p.) and sodium pentobarbital (20 mg/kg, i.p.). Tail flick reaction times were monitored and thermal hyperalgesia was induced by immersion of the tail in hot water at 55 degrees C for 1.5 min. In the groups of rats pretreated with saline (n = 5), 100 mg/kg D-NAME (n = 6), 10 (n = 5) or 25 (n = 6) mg/kg L-NAME, this thermal injury induced a transient reduction in the reaction time that was 54-59% of the baseline value. However, in the groups of rats pretreated with 50 (n = 6) or 100 (n = 7) mg/kg L-NAME the reaction times were 73.9 +/- 2.7% (P < 0.05) and 102.3 +/- 0.9% (P < 0.001) of the baseline values respectively, indicating a block of the hyperalgesic responses seen in the other groups. As this hyperalgesia has been reported to be blocked by NK-1 receptor antagonists, it is suggested that it is due to the action of endogenous substance P. In the second paradigm, tail flick responses were monitored in the awake rat and thermal hyperalgesia was induced by intrathecal administration of substance P (6.5 nmol) via a chronically implanted catheter.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Implication of a nitric oxide synthase mechanism in the action of substance P: L-NAME blocks thermal hyperalgesia induced by endogenous and exogenous substance P in the rat. 852 67

We tested whether NG-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide (NO) synthesis, can prevent interleukin 2 (IL-2)-induced capillary leakage in tumour-bearing mice without compromising the therapeutic benefits of IL-2. C3H/HeJ female mice transplanted s.c. with 2.5 x 10(5) C3-L5 mammary carcinoma cells were treated with: nothing, IL-2 (ten injections of 15,000 Cetus units i.p. every 8 h), L-NAME (0.1, 0.5, or 1 mg ml-1 drinking water), IL-2 + L-NAME (0.1 or 0.5 or 1 mg ml-1 drinking water). Therapies were given in one round (IL-2, days 10-13; L-NAME, days 9-13) or in two rounds (IL-2, days 10-13 and 20-23; L-NAME, days 9-13 and days 19-23) after tumour transplantation. Capillary leakage was measured from the water contents of the pleural cavities, lungs, spleen and kidneys. Effects of the therapies on the primary tumour size and the number of spontaneous lung metastases were also recorded. NO production was measured as the nitrite + nitrate levels in the serum and in the pleural effusion. After the first round of therapies, addition of L-NAME significantly reduced IL-2-induced pulmonary oedema and water retention in the spleen in a dose-dependent manner. It also significantly reduced the IL-2-induced rise in NO levels in the serum and pleural fluid, but did not affect IL-2-induced pleural effusion or water retention in the kidney. At later stages of tumour growth (day 23), tumours themselves induced significant fluid retention in the lungs and the kidney, which was not aggravated further with the second round of IL-2 therapy. At this time, L-NAME therapy alone ameliorated tumour-induced pulmonary oedema. During both rounds of therapy different doses of L-NAME alone caused a reduction of primary tumour growth as well as spontaneous lung metastases, which improved further with the addition of IL-2. The combination therapy was at least as effective as IL-2 therapy. In summary, L-NAME had anti-tumour effects in vivo, reduced the severity of IL-2-induced capillary leakage in some organs and did not compromise anti-tumour efficacy of IL-2 therapy. Thus, L-NAME could be a valuable adjunct to IL-2-based cancer therapy.
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PMID:NG-nitro-L-arginine methyl ester, an inhibitor of nitric oxide synthesis, ameliorates interleukin 2-induced capillary leakage and reduces tumour growth in adenocarcinoma-bearing mice. 854 5

The effect of chronic inhibition of nitric oxide (NO) biosynthesis has been investigated in two models of acute inflammation induced by carrageenin, i.e., paw oedema and pleurisy. Chronic inhibition of NO biosynthesis was achieved by including N omega-nitro-L-arginine methyl ester (L-NAME) in the drinking water to give a dose of approximately 75 mumol/rat/day for 2 and 4 weeks. Control animals received either tap water alone or the inactive enantiomer D-NAME. Since chronic NO inhibition increases blood pressure, rats made hypertensive (2 kidney-1 clip model; 2K-1C) were used to evaluate the effect of hypertension on the carrageenin-induced paw oedema. In a separate set of experiments, L-NAME-treated animals concomitantly received captopril (140 mumol/rat/day) to prevent hypertension. Animals chronically treated with L-NAME (but not D-NAME) for 2 and 4 weeks developed hypertension to the same extent as 2K-1C rats. Carrageenin-induced paw oedema was significantly reduced in animals chronically treated with L-NAME, but not with D-NAME or in 2K-1C rats. Subplantar injection of iloprost completely reversed the inhibition of paw oedema caused by L-NAME. Captopril (140 mumol/rat/day) significantly lowered the high blood pressure levels induced by L-NAME but did not significantly affect the inhibition of paw oedema caused by L-NAME. No changes in vascular permeability, as assessed by Evans blue extravasation, were observed in L-NAME-treated animals. The chronic treatment with L-NAME for 2 and 4 weeks did not inhibit carrageenin-induced leucocyte migration and fluid exudation into the pleural cavity. Although carrageenin-induced paw oedema is reduced in L-NAME-treated rats, this response reflects a decrease in local blood flow rather than an effect on vascular permeability.
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PMID:Effect of chronic nitric oxide synthesis inhibition on the inflammatory responses induced by carrageenin in rats. 856 27

The present experiments were designed to assess the effect of inhibiting NO synthesis on the renal failure induced in rats by treatment with high doses of gentamicin. Eighteen Wistar rats were given gentamicin 100 mg/kg body weight/day for 5 days, whereas another 18 rats were used as control. Half of the gentamicin-treated rats and half of the controls also received the specific inhibitor of NO synthesis, NG-nitro-L-arginine methyl ester (L-NAME), 0.05 mg/ml in the drinking water for 5 days. Arterial pressure and renal function were measured on the 5th day of the study. In the animals treated with L-NAME, arterial pressure was higher than in untreated rats, thus suggesting that the treatment was effective in inhibiting NO synthesis. Rats that received L-NAME and gentamicin, showed higher plasma creatinine levels and higher score of renal damage, as well as lower Na+ and K+ excretion and creatinine clearance than rats that received gentamicin alone. These data showing that NO inhibition aggravates gentamicin-induced renal failure, suggest that endogenously released NO plays a protective role in gentamicin nephrotoxicity.
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PMID:Effect of NG-nitro-L-arginine methyl ester on nephrotoxicity induced by gentamicin in rats. 856 55

The present study was designed to investigate the role of cardiopulmonary reflex, more specifically the Bezold-Jarisch reflex, in experimental hypertension induced by chronic administration of Nw-nitro-L-arginine methyl ester (L-NAME) (0.5 mg/ml) added to the drinking water for 6 days. The study was performed in male Wistar rats (200-350 g), 9 animals per group. L-NAME ingestion caused a significant increase in resting mean arterial pressure (MAP: 182 +/- 4 mmHg) and heart rate (HR: 447 +/- 20 bpm) when compared to untreated rats (MAP: 112 +/- 3 mmHg and HR: 355 +/- 10 bpm). Cardiopulmonary receptors were chemically stimulated with bolus injections of 5-hydroxytryptamine (5-HT, 4-10 micrograms/kg, iv) followed by measuring the falls in diastolic arterial pressure (DAP) and HR in conscious and freely moving animals. As expected, the responses to intravenous injections of 5-HT consisted of a dose-dependent reduction in HR (from 26 +/- 14 to 175 +/- 25 bpm) and DAP (from 7 +/- 4 to 39 +/- 3 mmHg) in the control rats. Both bradycardia and diastolic hypotension were significantly accentuated in the L-NAME animals (approximately 30%). These data suggest that, in contrast to other models of hypertension, in the present one caused by inhibition of nitric oxide synthesis, the Bezold-Jarisch reflex is exaggerated. This neural dysfunction could be related to changes in the cardiac vagal efferent or effector.
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PMID:Exaggerated Bezold-Jarisch reflex in the hypertension induced by inhibition of nitric oxide synthesis. 858 Aug 77

Chronic nitric oxide (NO) blockade promotes progressive hypertension, marked renal vasoconstriction, and glomerular and renal interstitial injury. Inhibition of the renin/angiotensin system prevents only partially the functional and structural abnormalities associated with this model. Because endothelin (ET) is a powerful endogenous vasoconstrictor and promitogen, we examined the hypothesis that it might also mediate the hemodynamic and renal structural effects of chronic NO blockade. Four groups of 16 adult male Munich-Wistar rats were studied. Group C received daily i.p. saline injections and no drug treatment. Group C+FR received daily i.p. injections of the ETA inhibitor FR139317, 32 mg/kg. Group NAME received the NO inhibitor N omega-nitro-L-arginine methyl ester (L-NAME), 65 mg/kg/day in the drinking water, and group NAME+FR received both L-NAME and FR139317. At 2 weeks of treatment, renal and systemic hemodynamic parameters assessed under anesthesia were similar in Groups C and C+FR. Rats of Group NAME exhibited systemic hypertension and renal vasoconstriction characteristic of this model. FR139317 was ineffective in preventing these abnormalities in Group NAME+FR. In eight additional rats of each group observed at 30 days, FR139317 treatment was equally inactive in the prevention of glomerular collapse and interstitial expansion, the two chief modalities of renal injury in this model. These results suggest that ET does not participate, at least via the ETA receptor, in the pathogenesis of hypertension, renal dysfunction, or renal injury associated with the chronic NO inhibition model.
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PMID:Do ETA receptors participate in the hemodynamic and renal effects of chronic nitric oxide blockade? 858 46

The aim of this study was to investigate in human skin in vivo the role of nitric oxide in maintaining resting vascular tone, in the vasodilatation caused by local warming and by ultraviolet B light exposure, and in the response to exogenous calcitonin gene-related peptide (CGRP). Cutaneous blood flow was assessed by planimetry of the visible erythema or pallor and by laser Doppler flowmetry. Intradermal injection of the inhibitor of nitric oxide synthase, NG-nitro-L-arginine methyl ester (L-NAME; 25 nmol), into forearm skin produced a visible pallor and a reduction of blood flow at a controlled ambient temperature of 21 degrees C. The control, NG-nitro-D-arginine methyl ester (D-NAME; 25 nmol) or NG-monomethyl-L-arginine (L-NMMA; 25 nmol) did not cause pallor or reduce blood flow. L-NAME and L-NMMA caused dose- and time-dependent increases in pallor, and reductions in cutaneous blood flow in skin that had been locally warmed by immersion in water at 45 degrees C and in skin that had been exposed to ultraviolet B light. D-NAME and D-NMMA at comparable concentrations did not have the effects on skin blood flow observed with the L forms. L-NAME and L-NMMA both inhibited the increased blood flow in human skin caused by the intradermal injection of CGRP (12.5 or 25 pmol). The reduction of CGRP-induced increase of blood flow by L-NAME was reversed by L-arginine. Neither D-NAME nor D-NMMA inhibited the increase in blood flow caused by CGRP. Neither L-NAME nor L-NMMA inhibited the increase in blood flow in human skin caused by the intradermal injection of prostaglandin E2 (63 pmol). The data show that nitric oxide is involved in the maintenance of resting blood flow in human skin and also in the cutaneous vasodilator responses to local warming, ultraviolet B irradiation, or injection of CGRP.
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PMID:Inhibitors of nitric oxide synthase in human skin. 859 60

The effect of the chronic oral application of NG-nitro-L-arginine methyl ester (L-NAME), a potent inhibitor of nitric oxide (NO) production, was studied on hypothalamic blood flow (HBF) and hypothalamic nitric oxide synthase (NOS) activity in rats. L-NAME was dissolved in the drinking water, in a concentration of 0.1 mg/ml, and was administered for 1 week. In the chronic L-NAME pretreated animals significantly reduced hypothalamic NOS activity and marked hypothalamic vasoconstriction were observed, the latter of which was counteracted by sustained systemic arterial hypertension, while HBF remained unchanged. The present model of chronic NOS blockade may be useful to assess the physiological functions of NO in the regulation of cerebral blood flow in the normally perfused brain.
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PMID:Hypothalamic blood flow remains unaltered following chronic nitric oxide synthase blockade in rats. 859 37

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