Inhibitors of nitric oxide synthesis block cold-induced thermogenesis in rats

2003 ◽  
Vol 81 (8) ◽  
pp. 834-838 ◽  
Author(s):  
Peter R Kamerman ◽  
Helen P Laburn ◽  
Duncan Mitchell
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Body Temperature ◽  
Nitric Oxide Synthase ◽  
Metabolic Rate ◽  
Water Loss ◽  
T Test ◽  
Evaporative Water Loss ◽  
Evaporative Water ◽  
Oxide Synthase

N-nitro-L-arginine methyl ester (L-NAME), an unspecific nitric oxide synthase inhibitor, was administered to individually caged Sprague–Dawley rats exposed to cold (18°C) and thermoneutral (30°C) environmental temperatures during the active phase of the animals' circadian cycle. Unrestrained rats were administered intraperitoneal injections of 100 mg·kg–1 L-NAME or 1 mL·kg–1 saline. Telemetry was used to measure abdominal temperature. On a separate occasion, metabolic rate and evaporative water loss were measured using indirect calorimetery, before and after the injection of 100 mg·kg–1 L-NAME, in rats exposed to the two environments. Injection of L-NAME had no significant effect on body temperature, metabolic rate, or evaporative water loss in rats exposed to the 30°C environment. In the 18°C environment, L-NAME injection caused a prolonged fall in body temperature (F(1,12) = 17.43, P = 0.001) and a significant decrease in metabolic rate (Student's t test, P = 0.001) and evaporative water loss (one-sample t test, P = 0.04). Therefore, the effects that systemic injection of L-NAME has on body temperature are dependent on environmental temperature, with nitric oxide synthase inhibition seemingly preventing the metabolic component of cold defence.Key words: N-nitro-L-arginine methyl ester, thermoregulation, telemetry, oxygen consumption.

Metabolism, Water-Balance and Temperature Regulation in the Golden Bandicoot (Isoodon-Auratus)

1992 ◽  
Vol 40 (5) ◽  
pp. 523 ◽  
Author(s):  
PC Withers
Keyword(s):  
Body Temperature ◽  
Water Balance ◽  
Metabolic Rate ◽  
Basal Metabolic Rate ◽  
Temperature Regulation ◽  
Water Loss ◽  
Thermal Conductance ◽  
Evaporative Water Loss ◽  
Evaporative Water ◽  
Low Rate

The Barrow I. golden bandicoot (Isoodon auratus) is a small arid-adapted marsupial. It has a low and labile body temperature, a low basal metabolic rate, a low thermal conductance, and a low rate of evaporative water loss. Its metabolic, thermal and hygric physiology resembles that of another arid-adapted bandicoot, the bilby, and differs from temperate and tropical bandicoots.

scholarly journals The role of ambient temperature and body mass on body temperature, standard metabolic rate and evaporative water loss in southern African anurans of different habitat specialisation

PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e7885 ◽  
Author(s):  
Mohlamatsane Mokhatla ◽  
John Measey ◽  
Ben Smit
Keyword(s):  
Body Temperature ◽  
Metabolic Rate ◽  
Body Mass ◽  
Water Loss ◽  
Standard Metabolic Rate ◽  
Evaporative Water Loss ◽  
Evaporative Water ◽  
Habitat Specialisation ◽  
Wide Range

Temperature and water availability are two of the most important variables affecting all aspects of an anuran’s key physiological processes such as body temperature (Tb), evaporative water loss (EWL) and standard metabolic rate (SMR). Since anurans display pronounced sexual dimorphism, evidence suggests that these processes are further influenced by other factors such as vapour pressure deficit (VPD), sex and body mass (Mb). However, a limited number of studies have tested the generality of these results across a wide range of ecologically relevant ambient temperatures (Ta), while taking habitat use into account. Thus, the aim of this study was to investigate the role of Ta on Tb, whole-animal EWL and whole-animal SMR in three wild caught African anuran species with different ecological specialisations: the principally aquatic African clawed frog (Xenopus laevis), stream-breeding common river frog (Amietia delalandii), and the largely terrestrial raucous toad (Sclerophrys capensis). Experiments were conducted at a range of test temperatures (5–35 °C, at 5 °C increments). We found that VPD better predicted rates of EWL than Ta in two of the three species considered. Moreover, we found that Tb, whole-animal EWL and whole-animal SMR increased with increasing Ta, while Tb increased with increasing Mb in A. delalandii and S. capensis but not in X. laevis. Whole-animal SMR increased with increasing Mb in S. capensis only. We did not find any significant effect of VPD, Mb or sex on whole-animal EWL within species. Lastly, Mb did not influence Tb, whole-animal SMR and EWL in the principally aquatic X. laevis. These results suggest that Mb may not have the same effect on key physiological variables, and that the influence of Mb may also depend on the species ecological specialisation. Thus, the generality of Mb as an important factor should be taken in the context of both physiology and species habitat specialisation.

Endothelium-dependent vasodilation of cerebral arteries is altered with simulated microgravity through nitric oxide synthase and EDHF mechanisms

2006 ◽  
Vol 101 (1) ◽  
pp. 348-353 ◽  
Author(s):  
Rhonda D. Prisby ◽  
M. Keith Wilkerson ◽  
Elke M. Sokoya ◽  
Robert M. Bryan ◽  
Emily Wilson ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Nitric Oxide Synthase ◽  
Cerebral Perfusion ◽  
Simulated Microgravity ◽  
Cerebral Arteries ◽  
Caveolin 1 ◽  
Fluid Shifts ◽  
Oxide Synthase

Cephalic elevations in arterial pressure associated with microgravity and prolonged bed rest alter cerebrovascular autoregulation in humans. Using the head-down tail-suspended (HDT) rat to chronically induce headward fluid shifts and elevate cerebral artery pressure, previous work has likewise shown cerebral perfusion to be diminished. The purpose of this study was to test the hypothesis that 2 wk of HDT reduces cerebral artery vasodilation. To test this hypothesis, dose-response relations for endothelium-dependent (2-methylthioadenosine triphosphate and bradykinin) and endothelium-independent (nitroprusside) vasodilation were determined in vitro in middle cerebral arteries (MCAs) from HDT and control rats. All in vitro measurements were done in the presence and absence of the nitric oxide synthase inhibitor NG-nitro-l-arginine methyl ester (10−5 M) and cyclooxygenase inhibitor indomethacin (10−5 M). MCA caveolin-1 protein content was measured by immunoblot analysis. Endothelium-dependent vasodilation to 2-methylthioadenosine triphosphate and bradykinin were both lower in MCAs from HDT rats. These lower vasodilator responses were abolished with NG-nitro-l-arginine methyl ester but were unaffected by indomethacin. In addition, HDT was associated with lower levels of MCA caveolin-1 protein. Endothelium-independent vasodilation was not altered by HDT. These results indicate that chronic cephalic fluid shifts diminish endothelium-dependent vasodilation through alterations in the endothelial nitric oxide synthase signaling mechanism. Such decrements in endothelium-dependent vasodilation of cerebral arteries could contribute to the elevations in cerebral vascular resistance and reductions in cerebral perfusion that occur after conditions of simulated microgravity in HDT rats.

The Nitric Oxide Synthase Inhibitor NG-nitro-L-Arginine Methyl Ester Potentiates Insulin Secretion Stimulated by Glucose and L-Arginine Independently of its Action on ATP-Sensitive K+ Channels

1998 ◽  
Vol 18 (1) ◽  
pp. 19-28 ◽  
Author(s):  
Albert Salehi ◽  
Fariborz Parandeh ◽  
Ingmar Lundquist
Keyword(s):  
Nitric Oxide ◽  
Insulin Secretion ◽  
Methyl Ester ◽  
Nitric Oxide Synthase ◽  
Insulin Release ◽  
Glucagon Secretion ◽  
Nitric Oxide Synthase Inhibitor ◽  
Insulin And Glucagon Secretion ◽  
Synthase Inhibitor ◽  
Oxide Synthase

The nature of the action of the nitric oxide synthase (NOS) inhibitor NG-nitro-L-arginine methyl ester (L-NAME) on hormone release from isolated islets was investigated. We found that glucose-induced insulin release was potentiated by L-NAME in the absence or presence of diazoxide, a potent K+ATP channel opener, as well as in the presence of diazoxide plus a depolarizing concentration of K+. At a low, physiological glucose concentration L-NAME did not influence insulin secretion induced by K+ but inhibited glucagon secretion. L-arginine-induced insulin release was potentiated by L-NAME. This potentiation was observed also in the presence of K+ plus diazoxide. Further, glucagon release induced by L-arginine as well as by L-arginine plus K+ and diazoxide was suppressed by L-NAME. The results strongly suggest that the L-NAME-induced potentiation of insulin secretion in response to glucose or L-arginine as well as the inhibitory effects on glucagon secretion are largely mediated by L-NAME directly suppressing islet NOS activity. Hence NO apparently affects insulin and glucagon secretion independently of membrane depolarization events.

Timing of Administration of Dexamethasone or the Nitric Oxide Synthase Inhibitor, Nitro-l-Arginine Methyl Ester, is Critical for Effective Treatment of Ischaemia-Reperfusion Injury to Rat Skeletal Muscle

1997 ◽  
Vol 93 (2) ◽  
pp. 167-174 ◽  
Author(s):  
Baimeng Zhang ◽  
Kenneth R. Knight ◽  
Bruce Dowsing ◽  
Elizabeth Guida ◽  
Long H. Phan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Methyl Ester ◽  
Nitric Oxide Synthase ◽  
Reperfusion Injury ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion ◽  
Nos Inhibitors ◽  
Oxide Synthase ◽  
Inducible Nos

1. The effects of the nitric oxide synthase (NOS) inhibitors, NG-nitro-l-arginine-methyl ester (l-NAME), nitroiminoethyl-l-ornithine and S-methylisothiourea on skeletal muscle survival following 2 h of tourniquet ischaemia and 24 h of reperfusion were compared with those of the antiinflammatory steroid, dexamethasone. 2. Administration of each of the NOS inhibitors or dexamethasone 30 min before reperfusion reduced the degree of skeletal muscle necrosis 24 h after reperfusion. 3. The influence of timing of drug administration was investigated. l-NAME administered 30 min before reperfusion, at 3 h after reperfusion, but not thereafter, significantly improved muscle survival compared with saline-treated controls. Dexamethasone administered 30 min before, or at 3 or 8 h after reperfusion, but not at 16 h, significantly improved muscle survival, but neither agent had protective effects when administered before ischaemia. 4. After 8 h of reperfusion of ischaemic skeletal muscle, cell-free homogenates contained Ca2+-independent (inducible) NOS activity which was reduced in dexamethasone-treated (2.5 mg/kg) rats. Furthermore, inducible NOS mRNA levels, as detected by reverse transcriptase-PCR, were increased after 8 h of reperfusion in saline, but not in dexamethasone-treated rats. 5. These data suggest a significant deleterious effect of endogenous NO which may be restricted to the first 3 h of the reperfusion phase of ischaemia-reperfusion injury, and raise the possibility of effective treatment of incipient reperfusion injury, even after several hours of reperfusion.

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