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

In the present study we evaluated the in vivo effect of arginine on CO(2) production from glucose in a medium with physiological and high extracellular K(+) concentrations. We also tested the influence of the nitric oxide synthase inhibitor, N(omega)-nitro-L-arginine methyl ester (L-NAME), on the effects elicited by arginine in order to investigate the possible participation of NO and/or its derivatives on the effects of arginine on CO(2) production from glucose. Sixty-day-old rats were treated with a single intraperitoneal injection of saline (control; group I), arginine (0.8 g/kg; group II), L-NAME (2.0 mg/kg; group III) or arginine (0.8 g/kg) plus L-NAME (2.0 mg/kg; group IV) and were killed 1 h later. Results showed that arginine administration inhibited CO(2) production from glucose at physiological extracellular K(+) concentration and L-NAME prevented such effect. In contrast, arginine administration had no effect on CO(2) production from glucose at high extracellular K(+) concentration. Based on these data, we also investigated the in vitro effect of arginine on CO(2) production from glucose in a medium with physiological extracellular K(+) concentration in hippocampus slices. Results showed that arginine (0.1-1.5 mM) when added to the incubation medium did not alter CO(2) production from glucose in hippocampus slices of untreated rats. In addition, we also demonstrated that arginine inhibits Na(+), K(+)-ATPase activity. The data indicate that the reduction of CO(2) production by arginine was probably mediated by NO and/or its derivatives, which could act inhibiting the activity of Na(+), K(+)-ATPase. The results suggest that arginine impairs energy metabolism in hippocampus slices of rats.
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PMID:Inhibition of CO(2) production from glucose by arginine in brain slices of rats. 1751 57

Adjustment of the Na/K ATPase activity to changes in oxygen availability is a matter of survival for neuronal cells. We have used freshly isolated rat cerebellar granule cells to study oxygen sensitivity of the Na/K ATPase function. Along with transport and hydrolytic activity of the enzyme we have monitored alterations in free radical production, cellular reduced glutathione, and ATP levels. Both active K(+) influx and ouabain-sensitive inorganic phosphate production were maximal within the physiological pO(2) range of 3-5 kPa. Transport and hydrolytic activity of the Na/K ATPase was equally suppressed under hypoxic and hyperoxic conditions. The ATPase response to changes in oxygenation was isoform specific and limited to the alpha1-containing isozyme whereas alpha2/3-containing isozymes were oxygen insensitive. Rapid activation of the enzyme within a narrow window of oxygen concentrations did not correlate with alterations in the cellular ATP content or substantial shifts in redox potential but was completely abolished when NO production by the cells was blocked by l-NAME. Taken together our observations suggest that NO and its derivatives are involved in maintenance of high Na/K ATPase activity under physiological conditions.
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PMID:Oxygen-induced Regulation of Na/K ATPase in cerebellar granule cells. 1789 92

We have previously demonstrated that acute arginine administration induces oxidative stress and compromises energy metabolism in rat hippocampus. In the present study, we initially investigated the effect of intracerebroventricular infusion of arginine (0.1, 0.5 and 1.5 mM solution) on Na(+),K(+)-ATPase activity and on some parameters of oxidative stress, namely thiobarbituric acid-reactive substances (TBA-RS) and total radical-trapping antioxidant parameter (TRAP) in the hippocampus of rats. Results showed that 1.5 mM arginine solution significantly increases TBA-RS and reduces Na(+),K(+)-ATPase activity and TRAP in the rat hippocampus. We also evaluated the influence of the nitric oxide synthase inhibitor, N(omega)-nitro-L-arginine methyl ester (L-NAME), and antioxidants, namely alpha-tocopherol plus ascorbic acid, on the effects elicited by arginine on Na(+),K(+)-ATPase activity, TBA-RS and TRAP. Results showed that treatment with alpha-tocopherol plus ascorbic acid per se did not alter these parameters but prevented these effects. Furthermore, intracerebroventricular infusion of L-NAME prevented the inhibition caused by arginine on Na(+),K(+)-ATPase activity, as well as the increased of TBA-RS. Our findings indicate that intracerebroventricular infusion of arginine induces oxidative stress in rat hippocampus and that the inhibition of Na(+),K(+)-ATPase activity caused by this amino acid was probably mediated by NO and/or its derivatives ONOO(-) and/or other free radicals. Finally, we suggest that the administration of antioxidants should be considered as an adjuvant therapy to specific diets in hyperargininemia.
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PMID:Protective effect of nitric oxide synthase inhibition or antioxidants on brain oxidative damage caused by intracerebroventricular arginine administration. 1819 Aug 96

The present study was focused on regulatory role of nitric oxide on functional properties of the cardiac Na, K-ATPase in three various animal models of hypertension: spontaneously hypertensive male rats (SHR) with increased activity of nitric oxide synthase (NOS) by 60 % (Sh1), SHR with decreased activity of NOS by 40 % (Sh2) and rats with hypertension induced by L-NAME (40 mg/kg/day) with depressed activity of NOS by 72 % (LN). Studying the utilization of energy substrate we observed higher Na, K-ATPase activity in the whole concentration range of ATP in Sh1 and decreased activity in Sh2 and LN. Evaluation of kinetic parameters revealed an increase of Vmax value by 37 % in Sh1 and decrease by 30 % in Sh2 and 17 % in LN. The KM value remained unchanged in Sh2 and LN, but was lower by 38 % in Sh1 indicating increased affinity of the ATP binding site, as compared to controls. During the activation with Na+ we observed increased Vmax by 64 % and increased KNa by 106 % in Sh1. In Sh2 we found decreased Vmax by 40 % and increased KNa by 38 %. In LN, the enzyme showed unchanged Vmax with increased KNa by 50 %. The above data indicate a positive role of increased activity of NOS in improved utilization of ATP as well as enhanced binding of Na+ by the cardiac Na, K-ATPase.
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PMID:Regulatory role of nitric oxide on the cardiac Na, K-ATPase in hypertension. 1837 97

This study aimed to investigate the vasoactivity of sulfur dioxide (SO2), a novel gas identified from vascular tissue, in rat thoracic aorta. The thoracic aorta was isolated, cut into rings, and mounted in organ-bath chambers. After equilibrium, the rings were gradually stretched to a resting tension. Isometric tension was recorded under the treatments with vasoconstrictors, SO2 derivatives, and various drugs as pharmacological interventions. In endothelium-intact aortic rings constricted by 1 microM phenylephrine (PE), SO2 derivatives (0.5-8 mM) caused a dose-dependent relaxation. Endothelium removal and a NOS inhibitor L-NAME reduced the relaxation to low doses of SO2 derivatives, but not that to relatively high doses (>or=2 mM). In endothelium-denuded rings, SO2 derivatives attenuated vasoconstriction induced by high K+ (60 mM) or CaCl2 (0.01-10 mM). The relaxation to SO2 derivatives in PE-constricted rings without endothelium was significantly inhibited by blockers of ATP-sensitive K+(KATP) and Ca2+-activated K+ (KCa) channels, but not by those of voltage-dependent K+ channels, Na+- K+-ATPase or Na+-Ca2+ exchanger. SO2 relaxed vessel tone via endothelium-dependent mechanisms associated with NOS activation, and via endothelium-independent mechanisms dependent on the inhibition of voltage-gated Ca2+ channels, and the opening of KATP and KCa channels.
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PMID:Sulfur dioxide relaxes rat aorta by endothelium-dependent and -independent mechanisms. 1865 3

Oscillatory contractile activity is an inherent property of blood vessels. Various cellular mechanisms have been proposed to contribute to oscillatory activity. Mouse small mesenteric arteries display a unique low frequency contractile oscillatory activity (1 cycle every 10-12 min) upon phenylephrine stimulation. Our objective was to identify mechanisms involved in this peculiar oscillatory activity. First-order mesenteric arteries were mounted in tissue baths for isometric force measurement. The oscillatory activity was observed only in vessels with endothelium, but it was not blocked by L-NAME (100 microM) or indomethacin (10 microM), ruling out the participation of nitric oxide and prostacyclin, respectively, in this phenomenon. Oscillatory activity was not observed in vessels contracted with K+ (90 mM) or after stimulation with phenylephrine plus 10 mM K+. Ouabain (1 to 10 microM, an Na+/K+-ATPase inhibitor), but not K+ channel antagonists [tetraethylammonium (100 microM, a nonselective K+ channel blocker), Tram-34 (10 microM, blocker of intermediate conductance K+ channels) or UCL-1684 (0.1 microM, a small conductance K+ channel blocker)], inhibited the oscillatory activity. The contractile activity was also abolished when experiments were performed at 20 degrees C or in K+-free medium. Taken together, these results demonstrate that Na+/K+-ATPase is a potential source of these oscillations. The presence of alpha-1 and alpha-2 Na+/K+-ATPase isoforms was confirmed in murine mesenteric arteries by Western blot. Chronic infusion of mice with ouabain did not abolish oscillatory contraction, but up-regulated vascular Na+/K+-ATPase expression and increased blood pressure. Together, these observations suggest that the Na+/K+ pump plays a major role in the oscillatory activity of murine small mesenteric arteries.
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PMID:A key role for Na+/K+-ATPase in the endothelium-dependent oscillatory activity of mouse small mesenteric arteries. 1982 Aug 82

The aim of the present study was to examine the effect of provinol, which is a mixture of polyphenolic compounds from red wine, on the secretion of catecholamines (CA) from isolated perfused rat adrenal medulla, and to elucidate its mechanism of action. Provinol (0.3~3 microg/ml) perfused into an adrenal vein for 90 min dose- and time-dependently inhibited the CA secretory responses evoked by ACh (5.32 mM), high K(+) (a direct membrane-depolarizer, 56 mM), DMPP (a selective neuronal nicotinic N(N) receptor agonist, 100 microM) and McN-A-343 (a selective muscarinic M(1) receptor agonist, 100 microM). Provinol itself did not affect basal CA secretion. Also, in the presence of provinol (1 microg/ml), the secretory responses of CA evoked by Bay-K-8644 (a voltage-dependent L-type dihydropyridine Ca(2+) channel activator, 10 microM), cyclopiazonic acid (a cytoplasmic Ca(2+)-ATPase inhibitor, 10 microM) and veratridine (an activator of voltage-dependent Na(+) channels, 10 microM) were significantly reduced. Interestingly, in the simultaneous presence of provinol (1 microg/ml) plus L-NAME (a selective inhibitor of NO synthase, 30 microM), the CA secretory responses evoked by ACh, high K(+), DMPP, McN-A-343, Bay-K-8644 and cyclpiazonic acid recovered to the considerable extent of the corresponding control secretion in comparison with the inhibition of provinol-treatment alone. Under the same condition, the level of NO released from adrenal medulla after the treatment of provinol (3 microg/ml) was greatly elevated in comparison to its basal release. Taken together, these data demonstrate that provinol inhibits the CA secretory responses evoked by stimulation of cholinergic (both muscarinic and nicotinic) receptors as well as by direct membrane-depolarization from the perfused rat adrenal medulla. This inhibitory effect of provinol seems to be exerted by inhibiting the influx of both calcium and sodium into the rat adrenal medullary cells along with the blockade of Ca(2+) release from the cytoplasmic calcium store at least partly through the increased NO production due to the activation of nitric oxide synthase.
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PMID:Provinol inhibits catecholamine secretion from the rat adrenal medulla. 1988 42

Resveratrol has been known to possess various potent cardiovascular effects in animal, but there is little information on its functional effect on the secretion of catecholamines (CA) from the perfused model of the adrenal medulla. Therefore, the aim of the present study was to determine the effect of resveratrol on the CA secretion from the isolated perfused model of the normotensive rat adrenal gland, and to elucidate its mechanism of action. Resveratrol (10~100microM) during perfusion into an adrenal vein for 90 min inhibited the CA secretory responses evoked by ACh (5.32 mM), high K(+) (a direct membrane-depolarizer, 56 mM), DMPP (a selective neuronal nicotinic N(n) receptor agonist, 100microM) and McN-A-343 (a selective muscarinic M(1) receptor agonist, 100microM) in both a time- and dose-dependent fashion. Also, in the presence of resveratrol (30microM), the secretory responses of CA evoked by veratridine 8644 (an activator of voltage-dependent Na(+) channels, 100microM), Bay-K-8644 (a L-type dihydropyridine Ca(2+) channel activator, 10microM), and cyclopiazonic acid (a cytoplasmic Ca(2+)-ATPase inhibitor, 10microM) were significantly reduced. In the simultaneous presence of resveratrol (30microM) and L-NAME (an inhibitor of NO synthase, 30microM), the CA secretory evoked by ACh, high K(+) , DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid were recovered to a considerable extent of the corresponding control secretion compared with the inhibitory effect of resveratrol alone. Interestingly, the amount of nitric oxide (NO) released from the adrenal medulla was greatly increased in comparison to its basal release. Taken together, these experimental results demonstrate that resveratrol can inhibit the CA secretory responses evoked by stimulation of cholinergic nicotinic receptors, as well as by direct membrane-depolarization in the isolated perfused model of the rat adrenal gland. It seems that this inhibitory effect of resveratrol is exerted by inhibiting an influx of both ions through Na(+) and Ca(2+) channels into the adrenomedullary cells as well as by blocking the release of Ca(2+) from the cytoplasmic calcium store, which are mediated at least partly by the increased NO production due to the activation of NO synthase.
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PMID:Resveratrol inhibits nicotinic stimulation-evoked catecholamine release from the adrenal medulla. 1996 50

The present study was attempted to investigate whether polyphenolic compounds isolated from wine, which is brewed from Rubus coreanum Miquel (PCRC), may affect the release of catecholamines (CA) from the isolated perfused adrenal medulla of the spontaneously hypertensive rats (SHRs), and to establish its mechanism of action. PCRC (20~180 microg/ml) perfused into an adrenal vein for 90 min relatively dose-dependently inhibited the CA secretory responses to ACh (5.32 mM), high K(+) (56 mM), DMPP (100 microM) and McN-A-343 (100 microM). PCRC itself did not affect basal CA secretion (data not shown). Also, in the presence of PCRC (60 microg/ml), the CA secretory responses to veratridine (a selective Na(+) channel activator (10 microM), Bay-K-8644 (a L-type dihydropyridine Ca(2+) channel activator, 10 microM), and cyclopiazonic acid (a cytoplasmic Ca(2+) -ATPase inhibitor, 10 microM) were significantly reduced, respectively. In the simultaneous presence of PCRC (60 microg/ml) and L-NAME (an inhibitor of NO synthase, 30 microM), the inhibitory responses of PCRC on the CA secretion evoked by ACh, high K(+), DMPP, and Bay-K-8644 were considerably recovered to the extent of the corresponding control secretion compared with that of PCRC-treatment alone. The level of NO released from adrenal medulla after the treatment of PCRC (60 microg/ml) was greatly elevated compared with the corresponding basal level. Taken together, these results demonstrate that PCRC inhibits the CA secretion from the isolated perfused adrenal medulla of the SHRs evoked by stimulation of cholinergic receptors as well as by direct membrane-depolarization. It seems that this inhibitory effect of PCRC is mediated by blocking the influx of calcium and sodium into the adrenal medullary chromaffin cells of the SHRs as well as by inhibition of Ca(2+) release from the cytoplasmic calcium store at least partly through the increased NO production due to the activation of NO synthase.
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PMID:Polyphenols of Rubus coreanum Inhibit Catecholamine Secretion from the Perfused Adrenal Medulla of SHRs. 2005 1

We investigated the effect of carbachol (CAR, a cholinergic agent) on intestinal mucosal blood flow (IMBF), activity of Na-K-ATPase, expression of aquaporin (AQP)-1, and intestinal absorption rate during enteral resuscitation of a 35%TBSA scald in rats with a glucose electrolyte solution (GES). One hundred male Wistar rats were randomly divided into five groups: sham scald (N group); scald without fluid resuscitation (S group); scald resuscitated with enteral GES alone (GES group); scald resuscitated with enteral CAR alone (CAR group); and scald resuscitated with enteral CAR plus GES (GES/CAR group). The rats were inflicted 35%TBSA third degree of scald injury on the back with boiling water (100 degrees C, 15 seconds) in all groups, except the sham scald group. A catheter was inserted into the proximal duodenum (5 cm distal to pylorus) and distal ileum (5 cm proximal to cecum), of each rats through laparotomy, thus a segment of intestine was virtually isolated to form a loop for inlet and outlet of introduced fluid. In N, GES, and GES/CAR groups, fluids were introduced 30 minutes after scald injury. The speed of fluid infusion was 4 ml/kg/1%TBSA for 4 hours. CAR (60 microg/kg) was injected into the intestinal lumen at 30-minute after injury in CAR and GES/CAR groups. At 2 and 4 hours after scald, intestinal absorption rate of water and Na, and IMBF were determined, respectively. Then, animals were killed, and specimens of intestinal tissue were obtained for the determination of the activity of Na-K-ATPase, hematoxylin-eosin coloring, and expression of AQP-1. The intestinal absorption rate was reduced markedly in GES group compared with sham scald group at 2 and 4 hours after scald, and absorption rate of small intestine in GES/CAR was significantly higher than that in GES group (P < .05). It was also found that there was significant decrease in IMBF, activity of Na-K-ATPase, and expression of AQP-1 in scald group compared with the sham group. However, in GES/CAR group, the levels of these parameters were significantly increased compared with scald groups (P < .05). The results indicate that CAR promotes intestinal absorption rate of water and Na by improving IMBF, ATPase activity, and AQP-1 expression in gut mucosa during resuscitation with enteral GES of burn shock in rats.
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PMID:Effect of carbachol on intestinal mucosal blood flow, activity of Na+-K+-ATPase, expression of aquaporin-1, and intestinal absorption rate during enteral resuscitation of burn shock in rats. 2006 57


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