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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study concerns the survival potential of mature neurons containing the enzyme nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase in the static slice culture of adult rat striatum. In the striatal tissues immediately after slicing, there was a scattered distribution of NADPH-diaphorase neurons stained in a Golgi-like manner, and the cell density of those neurons was 53 +/- 5 (mean +/- SEM; n = 10) cells per mm2. The time-sequential cell density analysis disclosed that the number of striatal NADPH-diaphorase neurons surviving after 1, 2, 4 and 6 day in culture were 26 +/- 5, 8 +/- 2, 5 +/- 2, and 3 +/- 2 (means +/- SEM; n = 10) cells per mm2, respectively. Thus, approximately 50% of striatal NADPH-diaphorase neurons survived for 1 day and a significant proportion of these neurons, although their number gradually decreased, were maintained in culture for at least several days. The conspicuous survival of the striatal NADPH-diaphorase neurons in slice culture is thought to reflect the damage-resistant natures of these cells.
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PMID:Survival of neurons containing the enzyme nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase in static slice cultures of adult rat striatum. 747 67

Nitric oxide (NO) is a short-lived radical species endowed with intercellular signalling functions in the mammalian brain. In the present study we have investigated the effects of focal injection into one inferior colliculus of N omega-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, on the acoustic middle latency responses (MLRs) evoked by click stimuli and recorded from the auditory cortex in anaesthetized rats. Microinfusion of L-NAME (1.0 mM) did not alter the latency of MLRs nor did it affect the evoked brain stem responses (ABRs). By contrast, L-NAME reduced P1a-N1 amplitude of MLRs by 51.7 +/- 6.6% (mean +/- SEM; n = 5) and almost complete recovery to background amplitude was obtained 15-25 min after treatment. The less active isomer, D-NAME (1.0 mM; n = 5), failed to produce consistent effects on the evoked MLRs. A higher concentration of L-NAME (5.0 mM; n = 5) yielded a 69.0 +/- 13.3% inhibition whereas maximum inhibition produced by 0.5 mM (n = 3) L-NAME was approximately equal to 10% of control value. The inhibitory effect typically evoked by 1.0 mM L-NAME was prevented by treating rats with L-arginine (5.0 mM; n = 5), the endogenous precursor of NO synthesis. Reduction of MLR amplitude was also obtained in rats receiving intracollicular injection of dizocilpine (MK801; 1.0 microM) and LY274614 (1.0 mM), two selective N-methyl-D-aspartate (NMDA) receptor antagonists. In conclusion, the present data support a role for intracollicular NO in the processing and transmission of the acoustic input to the auditory cortex in the rat.
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PMID:Possible modulation of auditory middle latency responses by nitric oxide in the inferior colliculus of anaesthetized rats. 750 Dec 86

The hypothesis that endogenous nitric oxide may play a physiological role in the regulation of carotid chemosensory activity was tested in this study. The nitric oxide synthase (NOS) inhibitors, L-nitro-arginine-methyl ester (L-NAME, 25-200 microM) and NG-monomethyl-L-arginine acetate (L-NMMA, 50 and 100 microM) were used to study its effects on the chemosensory activity of perfused and superfused cat carotid bodies (n = 21) in vitro at 37-37 degrees C. L-NAME elicited slow excitation of the sensory activity as did L-NMMA. The peak-response was dose-dependent, and approached saturation around 200 microM. The excitation by L-NAME showed the following characteristics (mean +/- SEM): latency of response, 2.2 min +/- 0.3 min; time to peak response, 5.5 min +/- 1.0 min and the peak response increased to 407 +/- 42 imp/sec from 88 +/- 13 imp/sec. The peak response was significantly different (P < 0.05) from the baseline activity. L-arginine (50-500 microM) only briefly reversed the stimulation. Hypoxia enhanced the excitation by L-NAME. On the other hand, sodium nitroprusside (SNP, 0.5-10 microM) which supplies NO, terminated the excitatory effect of L-NAME. The results provide evidence in favor of an inhibitory role of endogenous NO in the carotid body, and exogenous application of NO confirms the inhibitory effect.
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PMID:Nitric oxide-related inhibition of carotid chemosensory nerve activity in the cat. 752 21

We investigated mechanisms by which hypoxia produces relaxation of the aorta and tested the hypothesis that these mechanisms are altered during chronic hypertension. Tension of thoracic aortae from normotensive Wistar-Kyoto (WKY) rats and stroke-prone spontaneously hypertensive rats (SHRSP) was measured in an organ bath under control conditions and at two levels of hypoxia. In WKY rats, mild and severe hypoxia produced relaxation of the aortae (precontracted with phenylephrine) by 33 +/- 4% and 82 +/- 3%, respectively (mean +/- SEM). Removal of endothelium or administration of NG-nitro-L-arginine (10(-4) mol/L), an inhibitor of nitric oxide synthase, abolished relaxation of the aortae in response to mild hypoxia but did not affect relaxation during severe hypoxia. Glibenclamide (10(-6) mol/L), an inhibitor of potassium channels, attenuated relaxation of the aortae during mild and severe hypoxia by 49 +/- 16% and 74 +/- 4%, respectively. In SHRSP, mild hypoxia produced little relaxation of the aortae (3 +/- 4%, P < .05 compared with WKY). Indomethacin did not increase relaxation to mild hypoxia in SHRSP, which suggests that a cyclooxygenase-derived contracting factor does not contribute to impaired relaxation. Severe hypoxia relaxed the aortae by 86 +/- 4% in SHRSP, and glibenclamide inhibited this response by 60 +/- 9%. These findings suggest that relaxation of the aorta in response to mild hypoxia in WKY rats is mediated primarily by endothelium-derived relaxing factor, and the response to mild hypoxia is markedly impaired in SHRSP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relaxation of the aorta during hypoxia is impaired in chronically hypertensive rats. 753 13

Viral infection may induce the expression of nitric oxide (NO) synthase, resulting in increased NO formation that has an antiviral effect. NO may be produced by various cells of the upper and lower respiratory tract, and may be detected in the exhaled air. We have studied the levels of exhaled NO in 18 normal subjects during symptomatic upper respiratory tract infections and during recovery 3 weeks later. Exhaled NO was measured using a modified chemiluminescence analyser. At the time of symptoms of upper respiratory tract infection, the peak exhaled NO values were 315 +/- 57 ppb (mean +/- SEM) and decreased to 87 +/- 9 ppb during recovery. Recovery values of exhaled NO were similar to those reported in age-matched normal control subjects (88 +/- 3 ppb, n = 72). These findings suggest that symptomatic upper respiratory tract infections markedly increase the concentration of NO in exhaled air. This may reflect the induction of nitric oxide synthase (NOS) in upper and lower respiratory tract, and may be relevant to viral exacerbations of asthma.
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PMID:Increased nitric oxide in exhaled air of normal human subjects with upper respiratory tract infections. 753 34

1. Nitric oxide released from endothelial cells is a potent vasodilator that might play an important role in cardiovascular regulation during pregnancy. Platelets, like endothelial cells, contain a constitutive form of nitric oxide synthase. 2. The present study aimed to measure the activity of this nitric oxide-forming enzyme in normotensive pregnant and non-pregnant women, as well as in women who had developed pre-eclampsia. Nitric oxide synthase activity was measured in the platelets of 21 normotensive pregnant women, 16 non-pregnant women and seven pregnant women who had developed pre-eclampsia. 3. The nitric oxide synthase activity was significantly higher in normotensive pregnant women [36.8 +/- 2.7 pmol h-1 mg-1 of protein (mean +/- SEM), P < 0.001] than in non-pregnant control subjects (16.8 +/- 1.4 pmol h-1 mg-1 of protein) and in women with pre-eclampsia (24.5 +/- 2.1 pmol h-1 mg-1 of protein, P < 0.01). 4. These data suggest that nitric oxide synthesis is increased during normal pregnancy, possibly contributing to the vasodilatation associated with this condition. Nitric oxide generation, however, may be inappropriately low in pregnant women developing pre-eclampsia, thus leading to an enhanced vasoconstriction.
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PMID:Differential nitric oxide synthase activity in human platelets during normal pregnancy and pre-eclampsia. 754 94

Enhanced nitric oxide (NO) generation by stimulated NO synthase (NOS) activity may, through its oxidative metabolism contribute to tissue injury in experimental colitis. In this study the possible amelioration of experimental colitis by NG-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NOS activity, was evaluated. Colitis was induced in rats by intracolonic administration of 30 mg trinitrobenzene sulphonic acid (TNB) dissolved in 0.25 ml 50% ethanol or by flushing the colon of capsaicin pretreated rats with 2 ml of 5% acetic acid. In several experiments, L-NAME 0.1 mg/ml was added to the drinking water at the time of colitis induction with TNB or seven days before acetic acid treatment. Rats were killed at various time intervals after induction of colitis. A 10 cm distal colonic segment was isolated, weighed, lesion area measured, and explants organ cultured for 24 hours for determination of NO generation by the Greiss reaction. The rest of the mucosa was scraped for determination of myeloperoxidase and NOS activities and leukotriene generation. In TNB treated rats mean arterial pressure was also determined up to 72 hours after damage induction, with or without cotreatment with nitroprusside. L-NAME significantly decreased the extent of tissue injury in TNB treated rats. Seven days after TNB treatment lesion area was reduced by 55%, colonic weight by 37%, and myeloperoxidase and NOS activity by 59% and 42%, respectively. Acetic acid induced colitis in capsaicin pretreated rats was also significantly decreased by L-NAME. Twenty four hours after acetic acid treatment lesion area was reduced by 61%, colonic weight by 21% and NOS activity by 39%. Mean (SEM) arterial blood pressure in TNB+L-NAME treated rats was 37.6 (8.1) mm Hg higher than in TNB treated rats, an effect that was only partially abolished by nitroprusside. These results show that inhibition of NO synthesis by an L-arginine analogue significantly ameliorates the extent of tissue injury in two models of experimental colitis, an effect that is not due only to its vasoconstrictor properties. Modulation of NO generation may be a novel therapeutic approach in inflammatory bowel disease.
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PMID:Experimental colitis is ameliorated by inhibition of nitric oxide synthase activity. 867 8

Nebivolol, a beta 1 selective adrenergic receptor antagonist with additional properties, is a racemic mixture of (S,R,R,R)- and (R,S,S,S)-enantiomers. We investigated its effects on human forearm vasculature. Blood flow was measured using venous occlusion plethysmography during brachial artery infusion of drugs. Interaction between nebivolol and the L-arginine/nitric oxide pathway was investigated via comparison with carbachol (an endothelium-dependent agonist) and nitroprusside, and by coinfusion of a competitive inhibitor of nitric oxide synthase, NG-monomethyl L-arginine (LNMMA) +/- L-arginine. Nebivolol (354 micrograms/min) increased blood flow by 91 +/- 18% (mean +/- SEM, n = 8, P < .01) whereas an equimolar dose of atenolol had no significant effect. L-NMMA (1 mg/min) inhibited vasodilation to nebivolol (by 65 +/- 10%) and carbachol (by 49 +/- 8%) to a significantly greater extent than it reduced responses to nitroprusside. Inhibition of nebivolol response by L-NMMA was abolished by L-arginine (62 +/- 11% inhibition by L-NMMA, 15 +/- 17% inhibition by L-NMMA with L-arginine, 10 mg/min, n = 8). Vasodilation caused by the (S,R,R,R)- and (R,S,S,S)-enantiomers was similar. We conclude that nebivolol vasodilates human forearm vasculature via the L-arginine/nitric oxide pathway.
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PMID:Nebivolol vasodilates human forearm vasculature: evidence for an L-arginine/NO-dependent mechanism. 756 70

We tested the hypothesis that relaxation of the carotid artery during hypoxia is mediated by activation of glibenclamide-sensitive potassium channels and that this response is impaired in hyperlipidemic rabbits. In New Zealand White rabbits (plasma cholesterol, 69 +/- 12 mg/dL, mean +/- SEM) and Watanabe heritable hyperlipidemic (WHHL) rabbits (plasma cholesterol, 677 +/- 99 mg/dL), tension of the carotid artery was measured in an organ bath under control conditions and during two levels of hypoxia. In normal rabbits, mild hypoxia produced 21 +/- 2% relaxation in arteries precontracted with phenylephrine. Removal of endothelium or the nitric oxide synthase inhibitor NG-nitro-L-arginine (10(-4) mol/L) almost abolished relaxation in response to mild hypoxia in normal rabbits. Glibenclamide (10(-6) mol/L), an inhibitor of ATP-sensitive potassium channels, attenuated relaxation during mild hypoxia by almost 60%. In WHHL rabbits mild hypoxia relaxed the carotid artery by only 9 +/- 4% (P < .05 versus normal rabbits). Severe hypoxia produced greater relaxation of the carotid artery in normal than in WHHL rabbits (85 +/- 5% versus 52 +/- 8%, respectively, P < .05). Glibenclamide but not endothelial denudation or NG-nitro-L-arginine attenuated relaxation during severe hypoxia in normal and WHHL rabbits. Relaxation of the carotid artery to sodium nitroprusside was similar in normal and WHHL rabbits. These findings suggest that relaxation of the carotid artery in response to mild and severe hypoxia is impaired in WHHL rabbits and is mediated, in large part, by activation of glibenclamide-sensitive potassium channels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relaxation of the carotid artery to hypoxia is impaired in Watanabe heritable hyperlipidemic rabbits. 758 38

As a known vasodilator, nitric oxide (NO) probably acts by hyperpolarizing smooth muscle by increasing K conductance (GK). Therefore NO could mediate the anoxic hyperpolarizations of brain neurons that are also mediated by GK. We investigated this question by recording from CA1 neurons in submerged hippocampal slices (from rats), kept at 33 degrees C. Incubation with the NO synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME; 200 microM) had no significant effect on CA1 population spikes (delta = 2.5%, SEM +/- 3.1%, n = 7) or on the time course of their suppression by brief exposure to anoxia (2-3 min). In intracellular recordings, L-NAME did not change the resting membrane potential or input resistance (n = 10). In the presence of L-NAME, anoxic changes were not significantly different: the cells were hyperpolarized by 6.4 +/- 0.74 mV (6.3 +/- 0.82 mV for controls) and their resistance decreased by 16 +/- 3.2% (18 +/- 1.4% for controls, n = 10). In whole-cell recordings from another 15 cells (clamped at approximately -50 mV, near resting level), L-NAME also had no consistent effect on input conductase (GN) or holding current (IH); and the anoxic increased in GN were unchanged (44 +/- 12% before and 48 +/- 20% after, for n = 10). Thus NO does not appear to be a significant element in the mechanism of membrane and synaptic changes during brief anoxia in CA1 neurons in slices.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nitric oxide may be a mediator of effects of prolonged but not brief anoxia in CA1 neurons in slices. 762 65


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