The role of nitric oxide derived from l-arginine in the control of steroidogenesis, and perfusion medium flow rate in the isolated perfused rat adrenal gland

1993 ◽  
Vol 139 (3) ◽  
pp. 415-423 ◽  
Author(s):  
L. A. Cameron ◽  
J. P. Hinson
Keyword(s):  
Nitric Oxide ◽  
Adrenal Gland ◽  
Flow Rate ◽  
Adrenocortical Function ◽  
No Production ◽  
Percentage Increase ◽  
Perfusion Medium ◽  
Corticosterone Secretion ◽  
Dose Dependent

ABSTRACT The present studies were designed to investigate the role of nitric oxide (NO) in the regulation of adrenocortical function, using the intact rat adrenal gland in situ, perfused with medium (Hank's balanced salt solution) containing a range of concentrations of l-arginine, the substrate for NO production. In addition, the effects of NG-nitro-l-arginine methylester (l-NAME), an inhibitor of NO production, were investigated. Results showed that l-arginine caused a dose-dependent increase in the flow rate of the perfusion medium through the adrenal gland. This effect was specific, as neither d-arginine nor l-lysine had an effect. The presence of l-NAME (5 mmol/l) in perfusion medium containing l-arginine caused a decrease in flow rate to levels seen in the absence of l-arginine. In the presence of concentrations of l-arginine up to 500 μmol/l, corticosterone secretion rates were also stimulated in a dose-dependent manner. Further studies, investigating the effect of l-arginine on the response to ACTH(1–24) stimulation, found that the percentage increase in flow rate, aldosterone secretion and corticosterone secretion caused by ACTH were not significantly different using media containing 230 μmol l-arginine/l or in the absence of l-arginine. These results suggest a role for NO derived from l-arginine in the regulation of basal levels of adrenal vascular tone in the rat isolated adrenal gland preparation. They do not suggest an obligatory role for NO in either the vascular or steroidogenic response to ACTH stimulation. Journal of Endocrinology (1993) 139, 415–423

scholarly journals Effect of nitric oxide on rat adrenal zona fasciculata steroidogenesis

1998 ◽  
Vol 158 (2) ◽  
pp. 197-203 ◽  
Author(s):  
CB Cymeryng ◽  
LA Dada ◽  
EJ Podesta
Keyword(s):  
Nitric Oxide ◽  
Inhibitory Effect ◽  
Adrenocortical Function ◽  
Zona Fasciculata ◽  
Dependent Manner ◽  
Adrenal Cells ◽  
Corticosterone Secretion ◽  
Adrenal Zona Fasciculata ◽  
Dose Dependent

The present study was designed to investigate the role of nitric oxide (NO) in the regulation of adrenocortical function. Different NO donors, such as sodium nitroprusside (SNP), S-nitroso-L-acetyl penicillamine, diethylamine/NO complex sodium salt and diethylenetriamine NO adduct, significantly decreased corticosterone production both in unstimulated and in corticotropin-stimulated zone fasciculata adrenal cells, in a dose-dependent manner. The effect of SNP was reversed by ferrous hemoglobin. A selective inhibitor of NO synthase, L-NG-nitro-arginine significantly increased corticosterone secretion. The effect of SNP was not mediated by cGMP as permeable cGMP analogs did not reproduce its inhibitory effect. SNP significantly inhibited the steroidogenesis stimulated by 8Br-cAMP and 22(R)-OH-cholesterol, but was ineffective when corticosterone was produced in the presence of exogenously added pregnenolone. Moreover, the conversion of [3H]cholesterol to [3H]pregnenolone and the production of pregnenolone or progesterone (assessed by RIA) were significantly decreased by SNP. Taken together, these results suggest that NO may be a negative modulator of adrenal zona fasciculata steroidogenesis.

Viewing the ventromedial hypothalamus from the adrenal gland

1984 ◽  
Vol 246 (1) ◽  
pp. R1-R12 ◽  
Author(s):  
M. F. Dallman
Keyword(s):  
Circadian Rhythm ◽  
Insulin Secretion ◽  
Food Intake ◽  
Adrenal Gland ◽  
Ventromedial Hypothalamus ◽  
Adrenocortical Function ◽  
Suprachiasmatic Nuclei ◽  
Inhibit Food Intake ◽  
Dose Dependent

The relationships among food intake, insulin secretion, and adrenocortical function are reviewed. It is hypothesized that a major role of structures in, or passing through, the ventromedial hypothalamus is to inhibit food intake, insulin secretion, and adrenocortical function during the day (in the nocturnally active rat) and that this activity is normally driven by elements within the suprachiasmatic nuclei. Lesions of the ventromedial hypothalamus of rats result in nonrhythmic food intake, hyperinsulinemia, nonrhythmic adrenocortical function, and obesity. Adrenalectomy prevents or reverses the effects of lesions of the ventromedial hypothalamus on food intake, insulin secretion, and obesity, and corticosteroid replacement restores them. Because the actions of corticosteroids are both time- and dose-dependent, it is proposed that the effects of the tonic levels of corticosteroids observed after lesions of the ventromedial hypothalamus are to augment the hyperphagia, hyperinsulinemia, and substrate flow into fat to a greater extent than would occur if there were a normal circadian rhythm in adrenocortical function.

scholarly journals Role of nitric oxide in hypoxia inhibition of fever

1999 ◽  
Vol 87 (6) ◽  
pp. 2186-2190 ◽  
Author(s):  
Maria C. Almeida ◽  
Evelin C. Carnio ◽  
Luiz G. S. Branco
Keyword(s):  
Nitric Oxide ◽  
Treated Group ◽  
No Production ◽  
Significant Drop ◽  
Before And After ◽  
Synthase Inhibitor ◽  
Dose Dependent ◽  
Concomitant Exposure ◽  
Experimental Group

Hypoxia causes a regulated decrease in body temperature (Tb), and nitric oxide (NO) is now known to participate in hypoxia-induced hypothermia. Hypoxia also inhibits lipopolysaccharide (LPS)-induced fever. We tested the hypothesis that NO may participate in the hypoxia inhibition of fever. The rectal temperature of awake, unrestrained rats was measured before and after injection of LPS, with or without concomitant exposure to hypoxia, in an experimental group treated with N ω-nitro-l-arginine (l-NNA) for 4 consecutive days before the experiment and in a saline-treated group (control).l-NNA is a nonspecific NO synthase inhibitor that blocks NO production. LPS caused a dose-dependent typical biphasic rise in Tb that was completely prevented by hypoxia (7% inspired oxygen).l-NNA caused a significant drop in Tb during days 2–4 of treatment. When LPS was injected intol-NNA-treated rats, inhibition of fever was observed. Moreover, the effect of hypoxia during fever was significantly reduced. The data indicate that the NO pathway plays a role in hypoxia inhibition of fever.

The Signaling Pathways in Nitric Oxide Production by Neutrophils Exposed to N-nitrosodimethylamine

2018 ◽  
Vol 16 (2) ◽  
pp. 194-199
Author(s):  
Wioletta Ratajczak-Wrona ◽  
Ewa Jablonska
Keyword(s):  
Nitric Oxide ◽  
Signaling Pathways ◽  
Molecular Mechanisms ◽  
Polymorphonuclear Neutrophils ◽  
Microbial Pathogens ◽  
Human Neutrophils ◽  
No Production ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Background: Polymorphonuclear neutrophils (PMNs) play a crucial role in the innate immune system’s response to microbial pathogens through the release of reactive nitrogen species, including Nitric Oxide (NO). </P><P> Methods: In neutrophils, NO is produced by the inducible Nitric Oxide Synthase (iNOS), which is regulated by various signaling pathways and transcription factors. N-nitrosodimethylamine (NDMA), a potential human carcinogen, affects immune cells. NDMA plays a major part in the growing incidence of cancers. Thanks to the increasing knowledge on the toxicological role of NDMA, the environmental factors that condition the exposure to this compound, especially its precursors- nitrates arouse wide concern. Results: In this article, we present a detailed summary of the molecular mechanisms of NDMA’s effect on the iNOS-dependent NO production in human neutrophils. Conclusion: This research contributes to a more complete understanding of the mechanisms that explain the changes that occur during nonspecific cellular responses to NDMA toxicity.

Disruption of renal peritubular blood flow in lipopolysaccharide-induced renal failure: role of nitric oxide and caspases

2005 ◽  
Vol 289 (6) ◽  
pp. F1324-F1332 ◽  
Author(s):  
Manish M. Tiwari ◽  
Robert W. Brock ◽  
Judit K. Megyesi ◽  
Gur P. Kaushal ◽  
Philip R. Mayeux
Keyword(s):  
Nitric Oxide ◽  
Renal Failure ◽  
Blood Flow ◽  
Saline Group ◽  
No Production ◽  
Capillary Perfusion ◽  
Peritubular Capillary ◽  
Synthase Inhibitor ◽  
Peritubular Capillary Perfusion

Acute renal failure (ARF) is a frequent and serious complication of endotoxemia caused by lipopolysaccharide (LPS) and contributes significantly to mortality. The present studies were undertaken to examine the roles of nitric oxide (NO) and caspase activation on renal peritubular blood flow and apoptosis in a murine model of LPS-induced ARF. Male C57BL/6 mice treated with LPS ( Escherichia coli) at a dose of 10 mg/kg developed ARF at 18 h. Renal failure was associated with a significant decrease in peritubular capillary perfusion. Vessels with no flow increased from 7 ± 3% in the saline group to 30 ± 4% in the LPS group ( P < 0.01). Both the inducible NO synthase inhibitor l- N6-1-iminoethyl-lysine (l-NIL) and the nonselective caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp fluoromethylketone (Z-VAD) prevented renal failure and reversed perfusion deficits. Renal failure was also associated with an increase in renal caspase-3 activity and an increase in renal apoptosis. Both l-NIL and Z-VAD prevented these changes. LPS caused an increase in NO production that was blocked by l-NIL but not by Z-VAD. Taken together, these data suggest NO-mediated activation of renal caspases and the resulting disruption in peritubular blood flow are an important mechanism of LPS-induced ARF.

Nitrate reductases and hemoglobins control nitrogen-fixing symbiosis by regulating nitric oxide accumulation

2020 ◽  
Author(s):  
Antoine Berger ◽  
Alexandre Boscari ◽  
Alain Puppo ◽  
Renaud Brouquisse
Keyword(s):  
Nitric Oxide ◽  
Defense Responses ◽  
Nodule Formation ◽  
No Production ◽  
Degradation Pathways ◽  
Atmospheric Nitrogen ◽  
Metabolic Intermediate ◽  
Hypoxic Environment ◽  
Nitrate Reductases

Abstract The interaction between legumes and rhizobia leads to the establishment of a symbiotic relationship between plant and bacteria. This is characterized by the formation of a new organ, the nodule, which facilitates the fixation of atmospheric nitrogen (N2) by nitrogenase through the creation of a hypoxic environment. Nitric oxide (NO) accumulates at each stage of the symbiotic process. NO is involved in defense responses, nodule organogenesis and development, nitrogen fixation metabolism, and senescence induction. During symbiosis, either successively or simultaneously, NO regulates gene expression, modulates enzyme activities, and acts as a metabolic intermediate in energy regeneration processes via phytoglobin-NO respiration and the bacterial denitrification pathway. Due to the transition from normoxia to hypoxia during nodule formation, and the progressive presence of the bacterial partner in the growing nodules, NO production and degradation pathways change during the symbiotic process. This review analyzes the different source and degradation pathways of NO, and highlights the role of nitrate reductases and hemoproteins of both the plant and bacterial partners in the control of NO accumulation.

scholarly journals Recent insights into nitrite signaling processes in blood

2017 ◽  
Vol 398 (3) ◽  
pp. 319-329 ◽  
Author(s):  
Christine C. Helms ◽  
Xiaohua Liu ◽  
Daniel B. Kim-Shapiro
Keyword(s):  
Nitric Oxide ◽  
Human Physiology ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Nitrite Reduction ◽  
No Production ◽  
The Past ◽  
Acidic Conditions ◽  
Hypoxic Vasodilation

Abstract Nitrite was once thought to be inert in human physiology. However, research over the past few decades has established a link between nitrite and the production of nitric oxide (NO) that is potentiated under hypoxic and acidic conditions. Under this new role nitrite acts as a storage pool for bioavailable NO. The NO so produced is likely to play important roles in decreasing platelet activation, contributing to hypoxic vasodilation and minimizing blood-cell adhesion to endothelial cells. Researchers have proposed multiple mechanisms for nitrite reduction in the blood. However, NO production in blood must somehow overcome rapid scavenging by hemoglobin in order to be effective. Here we review the role of red blood cell hemoglobin in the reduction of nitrite and present recent research into mechanisms that may allow nitric oxide and other reactive nitrogen signaling species to escape the red blood cell.

Losartan Increases No Production from the Bovine Aortic Wall That is Stimulated by Angiotensin II

2003 ◽  
Vol 1 (3) ◽  
pp. 113-117 ◽  
Author(s):  
M. Myronidou ◽  
B. Kokkas ◽  
A. Kouyoumtzis ◽  
N. Gregoriadis ◽  
A. Lourbopoulos ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Angiotensin Ii ◽  
Aortic Wall ◽  
Vascular Wall ◽  
Protective Role ◽  
Normal Function ◽  
No Production ◽  
Chemical Inactivation

In these studies we investigated if losartan, an AT1- receptor blocker has any beneficial effect on NO production from the bovine aortic preparations in vitro while under stimulation from angiotensin II. Experiments were performed on intact specimens of bovine thoracic aorta, incubated in Dulbeco's MOD medium in a metabolic shaker for 24 hours under 95 % O2 and 5 % CO2 at a temperature of 37°C. We found that angiotensin II 1nM−10 μM does not exert any statistically significant action on NO production. On the contrary, angiotensin II 10nM increases the production of NO by 58.14 % (from 12.16 + 2.9 μm/l to 19.23 + 4.2 μm/l in the presence of losartan 1nM (P<0.05). Nitric oxide levels depend on both rate production and rate catabolism or chemical inactivation. Such an equilibrium is vital for the normal function of many systems including the cardiovascular one. The above results demonstrate that the blockade of AT1-receptors favors the biosynthesis of NO and indicate the protective role of losartan on the vascular wall.

Does autonomic blockade reveal a potent contribution of nitric oxide to locomotion-induced vasodilation?

2000 ◽  
Vol 279 (2) ◽  
pp. H726-H732 ◽  
Author(s):  
Don D. Sheriff ◽  
Christopher D. Nelson ◽  
Ryan K. Sundermann
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
No Production ◽  
Vascular Conductance ◽  
Absolute Level ◽  
Autonomic Blockade ◽  
The Absolute ◽  
Ganglionic Transmission ◽  
Treadmill Locomotion

We sought to test the role of nitric oxide (NO) in governing skeletal muscle (iliac) vascular conductance during treadmill locomotion in dogs ( n = 6; 3.2 and 6.4 km/h at 0% grade, and 6.4 km/h at 10% grade). As seen previously, the increase in muscle vascular conductance accompanying treadmill locomotion was little influenced by NO synthase inhibition alone with N ω-nitro-l-arginine methyl ester (l-NAME, 10 mg/kg iv), but the absolute value of conductance achieved during locomotion was reduced. Such ambiguous results provide an unclear picture regarding the importance of NO during locomotion. However, muscle vasodilation is normally restrained by the sympathetic system during locomotion. Thus a significant contribution by NO to the increase in vascular conductance that accompanies locomotion could be masked by partial withdrawal of the competing influence of sympathetic vasoconstrictor nerve activity secondary to the rise in arterial pressure following systemicl-NAME administration. To test this possibility, we compared the rise in muscle vascular conductance before and afterl-NAME treatment while ganglionic transmission was blocked by hexamethonium. Under these conditions, l-NAME significantly reduced both the rise in vascular conductance (by 32%, P < 0.001) and the absolute level of vascular conductance (by 30%, P < 0.001) achieved during locomotion with no effect on blood flow. Thus augmented NO production normally provides a significant drive to relax vascular smooth muscle in active skeletal muscle during locomotion. Potential deficits stemming from the absence of NO following l-NAME treatment are masked by less intense sympathetic restraint when autonomic function is intact.

scholarly journals Nitric Oxide Overproduction by cue1 Mutants Differs on Developmental Stages and Growth Conditions

Plants ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 1484 ◽  
Author(s):  
Tamara Lechón ◽  
Luis Sanz ◽  
Inmaculada Sánchez-Vicente ◽  
Oscar Lorenzo
Keyword(s):  
Nitric Oxide ◽  
Carbon Metabolism ◽  
Root Elongation ◽  
Developmental Stages ◽  
Primary Root ◽  
Carbon Sources ◽  
Growth Conditions ◽  
No Production

The cue1 nitric oxide (NO) overproducer mutants are impaired in a plastid phosphoenolpyruvate/phosphate translocator, mainly expressed in Arabidopsis thaliana roots. cue1 mutants present an increased content of arginine, a precursor of NO in oxidative synthesis processes. However, the pathways of plant NO biosynthesis and signaling have not yet been fully characterized, and the role of CUE1 in these processes is not clear. Here, in an attempt to advance our knowledge regarding NO homeostasis, we performed a deep characterization of the NO production of four different cue1 alleles (cue1-1, cue1-5, cue1-6 and nox1) during seed germination, primary root elongation, and salt stress resistance. Furthermore, we analyzed the production of NO in different carbon sources to improve our understanding of the interplay between carbon metabolism and NO homeostasis. After in vivo NO imaging and spectrofluorometric quantification of the endogenous NO levels of cue1 mutants, we demonstrate that CUE1 does not directly contribute to the rapid NO synthesis during seed imbibition. Although cue1 mutants do not overproduce NO during germination and early plant development, they are able to accumulate NO after the seedling is completely established. Thus, CUE1 regulates NO homeostasis during post-germinative growth to modulate root development in response to carbon metabolism, as different sugars modify root elongation and meristem organization in cue1 mutants. Therefore, cue1 mutants are a useful tool to study the physiological effects of NO in post-germinative growth.

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