scholarly journals Interaction among beta-endorphin, nitric oxide and prostaglandins during ovulation in rats

Reproduction ◽  
2003 ◽  
pp. 469-477 ◽  
Author(s):  
AG Faletti ◽  
C Mohn ◽  
M Farina ◽  
A Lomniczi ◽  
V Rettori
Keyword(s):  
Nitric Oxide ◽  
Prostaglandin E ◽  
Stimulatory Action ◽  
Beta Endorphin ◽  
Oxide Synthase ◽  
The Relationship ◽  
Ovulatory Process ◽  
Prostaglandin Synthesis Inhibitors ◽  
Enos Protein

The aim of this study was to investigate the relationship between beta-endorphin and nitric oxide (NO) during the ovulatory process in rats. Immature rats were treated with equine chorionic gonadotrophin-hCG to induce ovulation. An intrabursal injection of beta-endorphin stimulated nitric oxide synthase (NOS) activity. This effect was completely reversed when naltrexone was co-injected with beta-endorphin. The stimulatory action of beta-endorphin on NOS activity was studied to determine whether it was exerted via prostaglandins. Treatment with prostaglandin E(2) (PGE(2)) completely reversed the beta-endorphin-induced stimulation of NOS activity. Moreover, intrabursal injection of meloxicam, an inhibitor of cyclooxygenase 2, increased NOS activity, but this effect was not altered by co-injection with beta-endorphin. The presence of both endothelial NOS (eNOS) and inducible NOS (iNOS) in the ovary at 10 h after hCG treatment was studied by western blot analysis. Local administration of beta-endorphin inhibited the expression of eNOS protein, whereas expression of iNOS protein was not detectable. Ovarian beta-endorphin content was diminished at 10 h after hCG injection. Treatment with prostaglandin synthesis inhibitors in vivo augmented the ovarian beta-endorphin content. In conclusion, these results indicate that beta-endorphin stimulates the activity of ovarian NOS indirectly by inhibiting prostaglandin production.

Influence of exercise on dilatation of the basilar artery during diabetes mellitus

2004 ◽  
Vol 96 (5) ◽  
pp. 1730-1737 ◽  
Author(s):  
William G. Mayhan ◽  
Hong Sun ◽  
Jill F. Mayhan ◽  
Kaushik P. Patel
Keyword(s):  
Nitric Oxide ◽  
Diabetes Mellitus ◽  
Basilar Artery ◽  
Potential Role ◽  
Diabetic Rats ◽  
Cerebrovascular Reactivity ◽  
Oxide Synthase ◽  
Enos Protein

Our goal was to examine whether exercise training alleviates impaired nitric oxide synthase (NOS)-dependent dilatation of the basilar artery in Type 1 diabetic rats. To test this hypothesis, we measured in vivo diameter of the basilar artery in sedentary and exercised nondiabetic and diabetic rats in response to NOS-dependent (acetylcholine) and -independent (nitroglycerin) agonists. To determine the potential role for nitric oxide in vasodilatation in sedentary and exercised nondiabetic and diabetic rats, we examined responses after NG-monomethyl-l-arginine (l-NMMA). We found that acetylcholine produced dilatation of the basilar artery that was similar in sedentary and exercised nondiabetic rats. Acetylcholine produced only minimal vasodilatation in sedentary diabetic rats. However, exercise alleviated impaired acetylcholine-induced vasodilatation in diabetic rats. Nitroglycerin produced dilatation of the basilar artery that was similar in sedentary and exercised nondiabetic and diabetic rats. l-NMMA produced similar inhibition of acetylcholine-induced dilatation of the basilar artery in sedentary and exercised nondiabetic and diabetic rats. Finally, we found that endothelial NOS (eNOS) protein in the basilar artery was higher in diabetic compared with nondiabetic rats and that exercise increased eNOS protein in the basilar artery of nondiabetic and diabetic rats. We conclude that 1) exercise can alleviate impaired NOS-dependent dilatation of the basilar artery during diabetes mellitus, 2) the synthesis and release of nitric oxide accounts for dilatation of the basilar artery to acetylcholine in sedentary and exercised nondiabetic and diabetic rats, and 3) exercise may exert its affect on cerebrovascular reactivity during diabetes by altering levels of eNOS protein in the basilar artery.

Increased prostaglandin E generation and enhanced nitric oxide synthase activity in the non-insulin-dependent diabetic embryo during organogenesis

1998 ◽  
Vol 10 (2) ◽  
pp. 191 ◽  
Author(s):  
Alicia Jawerbaum ◽  
Elida T. Gonzalez ◽  
Virginia Novaro ◽  
Alicia Faletti ◽  
Debora Sinner ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Congenital Abnormalities ◽  
Prostaglandin E ◽  
No Donor ◽  
Insulin Dependent ◽  
Nos Inhibitor ◽  
Insulin Dependent Diabetic ◽  
Oxide Synthase

Embryonic development, prostaglandin E (PGE) generation and nitric oxide synthase (NOS) activity during organogenesis were evaluated in an experimental rat model of non-insulin- dependent diabetes (NIDD) generated by neonatal administration of streptozotocin. Gross malformations were detected in 5% of NIDD embryos and these embryos were all non-viable; in the other 95%, growth was retarded but no congenital abnormalities were found. Control embryos were all alive and not malformed. The NIDD 11-day embryos secreted more PGE into the incubation medium than did controls. The NO donor SIN–1 increased PGE production in both control and NIDD embryos. A NOS inhibitor (L-NMMA) reduced PGE generation in both experimental groups, suggesting a modulatory role of NO on embryonic PGE production. Activity of NOS was higher in NIDD 11-day embryos than in controls. Treatment in vivo of control and NIDD rats (Days 7–11 of gestation) with a NOS inhibitor (L-NAME; 5 mg kg-1 i.p.) reduced embryonic PGE production and induced a higher resorption rate and an increase in neural-tube defects. The results suggest that NO modulates PGE generation in the organogenetic embryo. In the NIDD model, overproduction of NO is observed, this NO probably enhancing embryonic PGE production. The relationship between PGE generation and the appearance of congenital abnormalities is discussed.

Nitric oxide in exhaled gas and tetrahydrobiopterin in plasma after exposure to hyperoxia

2020 ◽  
Vol 47 (1) ◽  
pp. 197-202
Author(s):  
Ronja Hesthammer ◽  
◽  
Stian Dahle ◽  
Jon Peder Storesund ◽  
Torunn Eide ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Healthy Subjects ◽  
Blood Samples ◽  
Time Points ◽  
Hyperoxic Exposure ◽  
Oxide Synthase ◽  
The Relationship

The fraction of nitric oxide in exhaled gas (FENO) is decreased after exposure to hyperoxia in vivo, although the mechanisms for this decrease is not clear. A key co-factor for nitric oxide synthase (NOS), tetrahydrobiopterin (BH4), has been shown to be oxidized in vitro when exposed to hyperoxia. We hypothesized that the decrease of FENO is due to decreased enzymatic generation of NO due to oxidation of BH4. The present study was performed to investigate the relationship between levels of FENO and plasma BH4 following hyperoxic exposure in humans. Two groups of healthy subjects were exposed to 100% oxygen for 90 minutes. FENO was measured before and 10 minutes (n = 13) or 60 minutes (n = 14) after the exposure. Blood samples were collected at the same time points for quantification of biopterin levels (BH4, BH2 and B) using LC-MS/MS. Each subject was his or her own control, breathing air for 90 minutes on a separate day. Hyperoxia resulted in a 28.6 % decrease in FENO 10 minutes after exposure (p < 0.001), confirming previous findings. Moreover, hyperoxia also caused a 14.2% decrease in plasma BH4 (p = 0.012). No significant differences were observed in the group measured 60 minutes after exposure. No significant correlation was found between the changes in FENO and BH4 after the hyperoxic exposure (r = 0.052, p = 0.795), this might be due to the recovery of BH4 being faster than the recovery of FENO.

scholarly journals Anti-Inflammatory Effects and Mechanisms ofFatsia polycarpaHayata and Its Constituents

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Hsueh-Ling Cheng ◽  
Nurkholis ◽  
Shi-Yie Cheng ◽  
Shen-Da Huang ◽  
Yan-Ting Lu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Interleukin 1 ◽  
Prostaglandin E ◽  
Extracellular Signal ◽  
Mitogen Activated Protein ◽  
Anti Inflammatory ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Fatsia polycarpa, a plant endemic to Taiwan, is an herbal medicine known for treating several inflammation-related diseases, but its biological function needs scientific support. Thus, the anti-inflammatory effects and mechanisms of the methanolic crude extract (MCE) ofF. polycarpaand its feature constituents, that is, brassicasterol (a phytosterol), triterpenoids 3α-hydroxyolean-11,13(18)-dien-28-oic acid (HODA), 3α-hydroxyolean-11-en-28,13β-olide (HOEO), fatsicarpain D, and fatsicarpain F, were investigated. MCE and HOEO, but not brassicasterol, dose-dependently inhibited lipopolysaccharide- (LPS-)induced expression of inducible nitric oxide synthase and cyclooxygenase-2 in RAW 264.7 macrophage line, whereas HODA, fatsicarpain D and fatsicarpain F were toxic to RAW cells. Additionally, MCE and HOEO suppressed LPS-induced production of nitric oxide, prostaglandin E2, and interleukin-1βand interfered with LPS-promoted activation of the inhibitor kappa B kinase (IKK)/nuclear factor-κB (NF-κB) pathway, and that of the mitogen-activated protein kinases (MAPKs) extracellular signal regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38. In animal tests, MCE and HOEO effectively ameliorated 12-O-tetradecanoylphorobol-13 acetate- (TPA-)induced ear edema of mice. Thus, MCE ofF. polycarpaexhibited an obvious anti-inflammatory activityin vivoandin vitrothat likely involved the inhibition of the IKK/NF-κB pathway and the MAPKs, which may be attributed by triterpenoids such as HOEO.

New aspects concerning to the characterization and the relationship with the immune response in vivo of the spiny lobster Panulirus argus nitric oxide synthase

Nitric Oxide ◽  
2011 ◽  
Vol 25 (4) ◽  
pp. 396-406 ◽  
Author(s):  
Tania Rodríguez-Ramos ◽  
Yamila Carpio ◽  
Laida Ramos ◽  
Tirso Pons ◽  
Omar Farnós ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Immune Response ◽  
Nitric Oxide Synthase ◽  
Spiny Lobster ◽  
Panulirus Argus ◽  
Oxide Synthase ◽  
The Relationship

scholarly journals Diterpenes from Euphorbia as Potential Leads for Drug Design

2008 ◽  
Vol 3 (6) ◽  
pp. 1934578X0800300 ◽  
Author(s):  
Elisa Barile ◽  
Gabriella Corea ◽  
Virginia Lanzotti
Keyword(s):  
Nitric Oxide ◽  
Binding Activity ◽  
Prostaglandin E ◽  
Plant Metabolites ◽  
Sar Studies ◽  
Tnf Α ◽  
Oxide Synthase ◽  
Rare Classes ◽  
First Time

In the course of our chemical survey of bioactive plant metabolites, a large number of diterpenes have been isolated from Euphorbia species that showed interesting pharmacological activities. In particular, over sixty jatrophane, modified jatrophane, segetane, pepluane, and paraliane diterpenoids, fifty of them reported for the first time, were extracted, purified and characterized from Euphorbia dendroides, E. characias, E. peplus, E. amygdaloides, and E. paralias. The compounds based on jatrophane and modified jatrophane skeletons were shown to be potent inhibitors of P-glycoprotein, a membrane protein that confers upon cells the ability to resist lethal doses of certain cytotoxic drugs by pumping them out of the cells, thus resulting in a reduced cytotoxic effect. Those belonging to the rare classes of pepluane and paraliane were shown to be promising anti-inflammatory agents in vivo. In addition, by using LPS-stimulated J774 murine macrophages, it was demonstrated that the effect is ascribable to the reduction in the production of nitric oxide, prostaglandin E2 and TNF-α by inhibiting the expression of inducible nitric oxide synthase, cyclooxygenase-2 and TNF-α mRNA, respectively, through the down-regulation of NF-κB binding activity. The isolation of structurally-related analogues allowed us to perform SAR studies, which gave information on the key pharmacophoric elements of these new classes of promising drugs.

Vasculoprotective Role of Inducible Nitric Oxide Synthase at Inflammatory Coronary Lesions Induced by Chronic Treatment With Interleukin-1β in Pigs in Vivo

Circulation ◽  
1997 ◽  
Vol 96 (9) ◽  
pp. 3104-3111 ◽  
Author(s):  
Yoshihiro Fukumoto ◽  
Hiroaki Shimokawa ◽  
Toshiyuki Kozai ◽  
Toshiaki Kadokami ◽  
Kouichi Kuwata ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Chronic Treatment ◽  
Interleukin 1Β ◽  
Coronary Lesions ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

scholarly journals Endothelial dysfunction and body mass index: is there a role for plasma peroxynitrite?

2021 ◽  
Vol 10 (1) ◽  
Author(s):  
Theresa Chikopela ◽  
Douglas C. Heimburger ◽  
Longa Kaluba ◽  
Pharaoh Hamambulu ◽  
Newton Simfukwe ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Endothelial Dysfunction ◽  
Body Mass ◽  
Vascular Function ◽  
Aortic Ring ◽  
Normal Weight ◽  
Oxide Synthase ◽  
Weight Groups

Abstract Background Endothelial function is dependent on the balance between vasoconstrictive and vasodilatory substances. The endothelium ability to produce nitric oxide is one of the most crucial mechanisms in regulating vascular tone. An increase in inducible nitric oxide synthase contributes to endothelial dysfunction in overweight persons, while oxidative stress contributes to the conversion of nitric oxide to peroxynitrite (measured as nitrotyrosine in vivo) in underweight persons. The objective of this study was to elucidate the interaction of body composition and oxidative stress on vascular function and peroxynitrite. This was done through an experimental design with three weight groups (underweight, normal weight and overweight), with four treatment arms in each. Plasma nitrotyrosine levels were measured 15–20 h post lipopolysaccharide (LPS) treatment, as were aortic ring tension changes. Acetylcholine (ACh) and sodium nitroprusside (SNP) challenges were used to observe endothelial-dependent and endothelial-independent vascular relaxation after pre-constriction of aortic rings with phenylephrine. Results Nitrotyrosine levels in saline-treated rats were similar among the weight groups. There was a significant increase in nitrotyrosine levels between saline-treated rats and those treated with the highest lipopolysaccharide doses in each of the weight groups. In response to ACh challenge, Rmax (percentage reduction in aortic tension) was lowest in overweight rats (112%). In response to SNP, there was an insignificantly lower Rmax in the underweight rats (106%) compared to the normal weight rats (112%). Overweight rats had a significant decrease in Rmax (83%) in response to SNP, signifying involvement of a more chronic process in tension reduction changes. A lower Rmax accompanied an increase in peroxynitrite after acetylcholine challenge in all weight groups. Conclusions Endothelial dysfunction, observed as an impairment in the ability to reduce tension, is associated with increased plasma peroxynitrite levels across the spectrum of body mass. In higher-BMI rats, an additional role is played by vascular smooth muscle in the causation of endothelial dysfunction.

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