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

Dopamine (DA) is released in large quantities from the striatum during cerebral ischemia. Along with excitatory neurotransmitters, DA plays a role in cellular neuronal ischemic injury. In this study we examined the role of nitric oxide (NO) in the ischemia-induced release of DA. A microdialysis probe was stereotactically placed into the corpus striatum of 16 Sprague-Dawley rats for DA, 3,4-dihydroxyphenylacetic acid (DOPAC), and homovanillic acid (HVA) level determinations. After probe stabilization, the animals received either NG-nitro-L-arginine-methyl ester (L-NAME), a NO synthase inhibitor, or vehicle through the microdialysis probe. Temporary global forebrain ischemia was induced using bilateral carotid artery ligature tightening and controlled hemorrhagic hypotension for 15 min. L-NAME administration caused a reduction in ischemic estimated extraneuronal DA concentration by 60% (P < 0.005) compared with control. There was an increase in both DOPAC and HVA concentrations during the recovery period compared to baseline values in the control group (P < 0.05). L-NAME also caused a reduction in HVA concentration compared to vehicle administration during the latter part of recovery (P < 0.05). These data support the concept that ischemic dopamine release may be mediated by NO. This NO-modulated DA release may contribute to the previously reported deleterious neurotoxic effects of NO during ischemia.
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PMID:Nitric oxide modulates dopamine release during global temporary cerebral ischemia. 776 37

1. Previously, we reported that noradrenaline (NA), in addition to its alpha 1-adrenoceptor-mediated contractile effect, may relax the rat small mesenteric artery (SMA) in order to account for steep Schild plots obtained with compounds classified as alpha 1-adrenoceptor antagonists. In this study, a relaxant action of NA has been exposed in the rat isolated, endothelium-denuded SMA precontracted by the thromboxane A2-mimetic, U46619. 2. NA, but not the selective alpha 2-adrenoceptor agonist, UK14304, produced concentration-dependent contraction of the SMA (pEC50 = 5.7 +/- 0.1). After precontraction with 0.1 microM U46619, 10 nM-30 microM NA produced a further contraction (pEC50 = 6.1 +/- 0.2), while higher concentrations of NA produced small, but significant, relaxant responses. 3. In the presence of 1 microM prazosin, 0.1-30 microM NA produced concentration dependent relaxation (pIC50 = 5.9 +/- 0.1) after precontraction with 0.1 microM U46619. The NA relaxation concentration-effect curve was completely inhibited by 1 microM of the beta 1/beta 2-adrenoceptor antagonist, timolol. However, when the concentration of prazosin was increased by 10 fold (10 microM), NA once again produced concentration-dependent relaxation (pIC50 = 4.5 +/- 0.2). This relaxation concentration-effect curve was not blocked by a 10 fold higher concentration of timolol (10 microM), nor by the presence of idazoxan (10 microM), cyanopindolol (10 microM), NG-nitro-L-arginine methyl ester (L-NAME, 100 microM), indomethacin (10 microM) or sulpiride (1 microM). However, haloperidol (10 microM) and (+/-)-SCH-23390 (10 nM) produced significant inhibition of the relaxation, suggesting the involvement of dopamine D1 receptors. 4. Dopamine also produced concentration-dependent relaxation following U46619 precontraction (pIC50 = 5.4 +/- 0.1) which was significantly inhibited by haloperidol and (+)-SCH-23390. Pretreatment with 10 microM phenoxybenzamine for 60 min produced a significant inhibition of the dopamine and NA relaxation curves and application of the operational model of agonism yielded estimates of the affinity (pKA = 5.3 +/- 0.2 and 4.4 +/- 0.2) and efficacy (log gamma = 0.06 +/- 0.11 and 0.01 +/- 0.10) for dopamine and NA, respectively, at D1 receptors. 5. HV723 (0.1 and 1 microM), a ligand that yielded a Schild plot slope parameter of unity as an antagonist of NA in the contractile assay, produced concentration-dependent inhibition of the NA-mediated relaxation (pA2 approximately 8). 6. The results of this study indicate that NA can activate D1 receptors mediating relaxation in the rat SMA at concentrations which were encountered in our previous receptor classification experiments using competitive alpha 1-adrenoceptor antagonists.
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PMID:Exposure and characterization of the action of noradrenaline at dopamine receptors mediating endothelium-independent relaxation of rat isolated small mesenteric arteries. 871 2

Dopamine (DA) is released in the medial preoptic area (MPOA) of male rats during copulation. DA agonists infused into the MPOA facilitate, and antagonists impair, copulatory behavior. Local administration of the nitric oxide (NO) precursor L-arginine also increases DA release in the MPOA. The present experiment used microdialysis to test whether NO promotes DA release during copulation. Males received either an NO synthesis inhibitor, nitro-L-arginine methyl ester (L-NAME, 400 microM), or its inactive isomer D-NAME (400 microM) into the MPOA via a microdialysis probe for 3 h prior to the introduction of a female. Following D-NAME administration, DA increased during copulation, while L-NAME prevented this increase. NO may therefore promote DA release in the MPOA of male rats, thereby facilitating copulation.
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PMID:Nitric oxide promotes medial preoptic dopamine release during male rat copulation. 905 47

Dopamine (DA) neurons in the ventral tegmental area and substantia nigra pars compacta were induced to fire in bursts with application of N-methyl-D-aspartate (NMDA, 20 microM) and apamin (100 nM) while recording intracellularly in the rat brain slice. L-Arginine (300 microM), a substrate for nitric oxide (NO) production, increased both the number of spikes per burst and the magnitude of interburst hyperpolarizations. Nitric oxide synthase inhibitors N-nitro-L-arginine methyl ester (L-NAME, 100 microM), N-nitro-L-arginine, and 7-nitroindazole inhibited NMDA-induced burst firing by reducing the number of spikes per burst. Moreover, L-arginine (100 microM) reversed the inhibition of burst firing produced by L-NAME. These findings suggest that NO facilitates NMDA-induced burst firing in DA neurons.
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PMID:Nitric oxide facilitates N-methyl-D-aspartate-induced burst firing in dopamine neurons from rat midbrain slices. 983 90

Dopamine and dopamine-1 receptor agonists produce diuresis and natriuresis by causing changes in renal hemodynamics and by the activation of dopamine-1 receptors located within the various regions of the nephron. Nitric oxide plays an important role in the maintenance of systemic and regional hemodynamics. The present study was undertaken to investigate the effect of locally generated nitric oxide on renal function and its potential influence on the renal responses to dopamine-1 receptor agonists. The intrarenal infusion of a nitric oxide synthase inhibitor, L-NAME, (50 microg/kg min for 90 min) in anesthetized rats produced significant decreases in urine volume, urinary sodium excretion, glomerular filtration rate and fractional sodium excretion. These changes in renal function were associated with a concomitant decrease in urinary nitrate excretion, an indicator of nitric oxide release. However, L-NAME at this dose did not produce any significant changes in mean arterial pressure or heart rate. Intravenous infusion of fenoldopam (1 microg/kg min for 30 min), a selective dopamine-1 receptor agonist, produced diuresis and natriuresis without causing any changes in mean arterial pressure and heart rate. These renal effects of fenoldopam were significantly attenuated in animals that received the simultaneous infusion of L-NAME (intrarenal). Similar results were obtained with dopamine in that the natriuretic and diuretic response to dopamine was also attenuated during simultaneous infusion of dopamine with L-NAME. In addition, the diuresis and natriuresis produced by fenoldopam and dopamine was associated with increases in urinary nitrate excretion. Interestingly, these increases in the nitrate levels seen with fenoldopam and dopamine were also significantly reduced in the presence of L-NAME. These results indicate that intrarenal nitric oxide plays an important role in regulating renal sodium excretion and that an intact renal nitric oxide system is required for the full expression of diuretic and natriuretic response seen during dopamine-1 receptor activation.
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PMID:The role of intrarenal nitric oxide in the natriuretic response to dopamine-receptor activation. 1080 36

We examined the effect of N(G)-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase (NOS) inhibitor, on extracellular potassium ion concentration ([K(+)](o))-enhanced hydroxyl radical (.OH) generation due to 1-methyl-4-phenylpyridinium ion (MPP(+)) was examined in the rat striatum. Rats were anesthetized, and sodium salicylate in Ringer's solution (0.5 nmol/microl per min) was infused through a microdialysis probe to detect the generation of.OH as reflected by the non-enzymatic formation of 2,3-dihydroxybenzoic acid (DHBA) in the striatum. Induction of KCl (20, 70 and 140 mM) increased MPP(+)-induced.OH formation trapped as 2,3-dihydroxybenzoic acid (DHBA) in a concentration dependent manner. However, the application of L-NAME (5 mg/kg i.v.) abolished the [K(+)](o) depolarization-induced.OH formation with MPP(+). Dopamine (DA; 10 microM) also increased the levels of DHBA due to MPP(+). However, the effect of DA after application of L-NAME did not change the levels of DHBA. On the other hand, the application of allopurinol (20 mg/kg i.v., 30 min prior to study), a xanthine oxidase (XO) inhibitor was abolished the both [K(+)](o)- and DA-induced.OH generation. Moreover, when iron(II) was administered to MPP(+) then [K(+)](o) (70 mM)-pretreated animals, a marked increase in the level of DHBA. However, when corresponding experiments were performed with L-NAME-pretreated animals, the same results were obtained. Therefore, NOS activation may be no relation to Fenton-type reaction via [K(+)](o) depolarization-induced.OH generation. The present results suggest that [K(+)](o)-induced depolarization augmented MPP(+)-induced.OH formation by enhancing NO synthesis.
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PMID:Nitric oxide enhances MPP(+)-induced hydroxyl radical generation via depolarization activated nitric oxide synthase in rat striatum. 1138 16

Dopamine (DA) release in the medial preoptic area (MPOA) of the hypothalamus is an important facilitator of male sexual behavior. The presence of a receptive female increases extracellular DA in the MPOA, which increases further during copulation. However, the neurochemical events that mediate the increase of DA in the MPOA are not fully understood. Here we report that glutamate, reverse-dialyzed into the MPOA, increased extracellular DA, which returned to baseline after the glutamate was removed. This increase was prevented by co-administration of the nitric oxide synthase inhibitor NG-nitro-l-arginine methyl ester (L-NAME), but not by the inactive isomer, Nw-nitro-d-arginine methyl ester (D-NAME). In contrast, extracellular concentrations of the major metabolites of DA were decreased by glutamate, suggesting that the DA transporter was inhibited. These decreases were also inhibited by L-NAME, but not D-NAME. These results indicate that glutamate enhances extracellular DA in the MPOA, at least in part, via nitric oxide activity. Therefore, glutamatergic stimulation of nitric oxide synthase may generate the female-induced increase in extracellular DA in the MPOA, which is important for the expression of male sexual behavior.
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PMID:Nitric oxide mediates glutamate-evoked dopamine release in the medial preoptic area. 1505 Nov 59

Dopamine in the medial preoptic area (MPOA) facilitates copulation in male rats, and nitric oxide (NO) regulates basal and female-stimulated MPOA dopamine release. Microinjection of L-nitro-arginine methyl ester (L-NAME, an NO synthesis inhibitor) into the MPOA blocked copulation in naive rats and impaired copulation in sexually experienced males. In other naive rats, L-NAME or saline was microinjected into the MPOA before each of 7 daily exposures to a receptive female placed over their cage. In a drug-free test on Day 8, copulation by L-NAME-treated rats was similar to that of unexposed controls and was impaired relative to saline-treated males. Therefore, NO in the MPOA is important for copulation and stimulus sensitization in male rats.
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PMID:A nitric oxide synthesis inhibitor in the medial preoptic area inhibits copulation and stimulus sensitization in male rats. 1559 60

Pieces of gill isolated from the clam Mercenaria mercenaria clear colloidal graphite from seawater, and the clearance rates are measurable. 5-Hydroxytryptamine (5-HT) had a biphasic effect on clearance rates: concentrations from 10(-6) to 10(-5) mol l(-1) 5-HT increased clearance, but higher concentrations reduced it. During the summer, the gills were less responsive to 5-HT: the threshold increased from 1 x 10(-6) to 5 x 10(-6) mol l(-1), and although the rate was still maximal at 10(-5) mol l(-1), it was significantly lower than the maximal rate in the winter. At 10(-5) mol l(-1) 5-HT, which maximized clearance, the lateral cilia were active, the interfilament space decreased and the diameter of the water tubes increased. Higher concentrations of 5-HT contracted the gill musculature, which inhibited the lateral cilia, decreased the interfilament space even more and decreased the diameter of the water tubes. The nitric oxide (NO) generator DEANO stimulated clearance in the winter but had no effect during the summer. L-NAME, an inhibitor of NO synthesis, diminished the effect of 5-HT during the winter but was ineffective during the summer. The diminished response to 5-HT of winter gills treated with L-NAME was statistically equal to the response of the gills to 5-HT during the summer. Dopamine (DA) inhibited clearance, and the gills were more sensitive to DA in winter than in summer. Microscopic examination of untreated gills revealed little or no lateral ciliary activity, and clearance was minimal. Thus, clearance rates of isolated gills behave in a manner consistent with the seasonality and pharmacology of the lateral cilia and branchial musculature.
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PMID:Seasonal control of particle clearance by isolated gills from the clam Mercenaria mercenaria. 1760 56

Dopamine (DA) released from lateral olivocochlear (LOC) terminals may have a neuroprotective effect in the cochlea. To explore the role of N-methyl-d-aspartate (NMDA) receptors and nitric oxide (NO) in the modulation of a cochlear DA release, we measured the release of [3H]DA from isolated mouse cochlea in response to the application of NMDA. NMDA at 100 muM significantly increased the electrical-field stimulation-evoked and resting release of DA from the cochlea. The NO donor sodium nitroprusside enhanced the basal outflow of DA but failed to influence the evoked release. The administration of the nitric oxide synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME) alone was ineffective, but it significantly inhibited the initial phase of the NMDA-induced elevation of DA outflow, which suggested the role of NO in the NMDA-induced DA release. The DA uptake inhibitor nomifensine increased the electrically evoked release of DA. Nomifensine failed to change the effect of NMDA on the resting or electrically-evoked DA release, which suggested that the uptake mechanism does not play a role in NMDA-evoked and NO-mediated DA release. In summary, we provide evidence that NO can modulate the release of DA from the cochlea following NMDA receptor activation, but does not affect the uptake of DA.
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PMID:The role of N-methyl-D-aspartate receptors and nitric oxide in cochlear dopamine release. 1846 86


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