scholarly journals Growth-related changes in the influence of nitric oxide on arteriolar tone

1999 ◽  
Vol 277 (4) ◽  
pp. H1570-H1578 ◽  
Author(s):  
J. R. Linderman ◽  
M. A. Boegehold
Keyword(s):  
Nitric Oxide ◽  
Age Groups ◽  
Prostaglandin E ◽  
Similar Amount ◽  
Juvenile Growth ◽  
Juvenile Rats ◽  
Age Related ◽  
Weanling Rats ◽  
Arteriolar Tone

This study was designed to determine whether juvenile growth is accompanied by changes in the local influence of nitric oxide (NO) or prostaglandins on arteriolar tone. In vivo microscopy was used to study proximal arterioles in the spinotrapezius muscle of rats 4–5 wk (weanling), 7–8 wk (juvenile), and 11–12 wk (mature) of age. From 4 to 12 wk of age, arterioles underwent an increase in resting diameter (from 31 ± 2 to 49 ± 2 μm) and volume flow (from 7 ± 1 to 10 ± 1 nl/s) but a decrease in resting wall shear rate (from 1,901 ± 150 to 748 ± 50 s−1). NO synthase inhibition with N G-monomethyl-l-arginine (l-NMMA) had no effect on arteriolar diameters in weanling rats but reduced diameters by 14 ± 4% in juvenile rats and by 13 ± 4% in mature rats. Cyclooxygenase inhibition with meclofenamate reduced arteriolar diameters by a similar amount (13 ± 4 to 18 ± 3%) in all age groups. There were no age-related differences in arteriolar responsiveness to locally applied sodium nitroprusside or prostaglandin E2. Arteriolar responsiveness to ACh was also similar in all groups, but thel-NMMA-sensitive portion of this response was smaller in mature rats than in weanling rats. Elevation of flow-related shear stress caused arteriolar dilation in juvenile rats but not in weanling rats. These findings suggest that arteriolar smooth muscle responsiveness to NO or prostaglandins does not change during juvenile growth and that basally released vasodilator prostaglandins exert a constant influence on arteriolar tone throughout this period. Basal NO activity also modulates arteriolar tone in juvenile and mature rats but not in weanling rats. In contrast, agonist-stimulated NO release is prominent in weanling and juvenile rats but somewhat decreased in mature rats, where cyclooxygenase products also contribute to ACh induced dilation.

Longitudinal force and stress of rat's esophagus: age-related changes.

1977 ◽  
Vol 232 (6) ◽  
pp. E580
Author(s):  
M P Zabinski ◽  
P Biancani
Keyword(s):  
Age Groups ◽  
Longitudinal Direction ◽  
Longitudinal Force ◽  
Active Stress ◽  
Length Relationship ◽  
Age Related ◽  
Old Rats ◽  
The Difference

Longitudinal force-length relationship of the rat esophagus was studied in vitro in three age groups: 1 mo, 3 mo, and 12 mo. The length of maximum force development (MFD) occurs at 1.4-1.5 times the in vivo length for all age groups. The active force developed at MFD increases markedly with age. The difference in the active forces in the 3-mo and 12-mo age groups is due to differences in cross section because the active stress of the esophagus in the longitudinal direction is approximately equal for the two age groups. The active stress in the 1-mo-old rats is lower than in the 3-mo-old rats, suggesting an increased contractility of the esophagus with age in this period of development.

scholarly journals In vitro and in vivo anti-inflammatory activities of a sterol-enriched fraction from freshwater green alga, Spirogyra sp.

2020 ◽  
Vol 23 (1) ◽  
Author(s):  
Lei Wang ◽  
You-Jin Jeon ◽  
Jae-Il Kim
Keyword(s):  
Nitric Oxide ◽  
Green Alga ◽  
Raw 264.7 Cells ◽  
Ros Generation ◽  
Prostaglandin E ◽  
No Production ◽  
Raw 264.7 ◽  
Anti Inflammatory

Abstract Background Inflammation plays a crucial role in the pathogenesis of many diseases such as arthritis and atherosclerosis. In the present study, we evaluated anti-inflammatory activity of sterol-rich fraction prepared from Spirogyra sp., a freshwater green alga, in an effort to find bioactive extracts derived from natural sources. Methods The sterol content of ethanol extract of Spirogyra sp. (SPE) was enriched by fractionation with hexane (SPEH), resulting 6.7 times higher than SPE. Using this fraction, the in vitro and in vivo anti-inflammatory activities were evaluated in lipopolysaccharides (LPS)-stimulated RAW 264.7 cells and zebrafish. Results SPEH effectively and dose-dependently decreased the production of nitric oxide (NO) and prostaglandin E2 (PGE2). SPEH suppressed the production of pro-inflammatory cytokines including interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and IL-1β through downregulating nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression in LPS-stimulated RAW 264.7 cells without cytotoxicity. The in vivo test results indicated that SPEH significantly and dose-dependently reduced reactive oxygen species (ROS) generation, cell death, and NO production in LPS-stimulated zebrafish. Conclusions These results demonstrate that SPEH possesses strong in vitro and in vivo anti-inflammatory activities and has the potential to be used as healthcare or pharmaceutical material for the treatment of inflammatory diseases.

scholarly journals Inhibitory Effects of Traditional Herbal Formula Pyungwi-San on Inflammatory ResponseIn VitroandIn Vivo

2013 ◽  
Vol 2013 ◽  
pp. 1-19 ◽  
Author(s):  
Ji Young Cha ◽  
Ji Yun Jung ◽  
Jae Yup Jung ◽  
Jong Rok Lee ◽  
Il Je Cho ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Mediators ◽  
Raw 264.7 Cells ◽  
Prostaglandin E ◽  
Herbal Formula ◽  
Paw Edema ◽  
Cox 2 ◽  
Anti Inflammatory

Pyungwi-san (PWS) is a traditional basic herbal formula. We investigated the effects of PWS on induction of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), pro-inflammatory cytokines (interleukin-6 (IL-6) and tumor necrosis factor-α(TNF-α)) and nuclear factor-kappa B (NF-κB) as well as mitogen-activated protein kinases (MAPKs) in lipopolysaccharide-(LPS-) induced Raw 264.7 cells and on paw edema in rats. Treatment with PWS (0.5, 0.75, and 1 mg/mL) resulted in inhibited levels of expression of LPS-induced COX-2, iNOS, NF-κB, and MAPKs as well as production of prostaglandin E2(PGE2), nitric oxide (NO), IL-6, and TNF-αinduced by LPS. Our results demonstrate that PWS possesses anti-inflammatory activities via decreasing production of pro-inflammatory mediators through suppression of the signaling pathways of NF-κB and MAPKs in LPS-induced macrophage cells. More importantly, results of the carrageenan-(CA-) induced paw edema demonstrate an anti-edema effect of PWS. In addition, it is considered that PWS also inhibits the acute edematous inflammations through suppression of mast cell degranulations and inflammatory mediators, including COX-2, iNOS and TNF-α. Thus, our findings may provide scientific evidence to explain the anti-inflammatory properties of PWSin vitroandin vivo.

Age-related changes in carotid vascular responses to adenosine and nitric oxide in the rat: in vitro and in vivo studies

2010 ◽  
Vol 109 (2) ◽  
pp. 305-313 ◽  
Author(s):  
Nisreen Mansour Omar ◽  
Janice M. Marshall
Keyword(s):  
Carotid Artery ◽  
Cerebral Autoregulation ◽  
No Synthase ◽  
Aged Rats ◽  
Middle Aged ◽  
Juvenile Rats ◽  
Age Related ◽  
Carotid Circulation

We investigated how the ability of adenosine to release nitric oxide (NO) from carotid artery in vitro, and dilator responses evoked in carotid circulation in vivo by systemic infusion of adenosine, change with age in rats of 4–5, 10–12, and 42–44 wk (juvenile, mature, and middle aged). A secondary aim was to follow age-related changes in carotid/cerebral autoregulation. In opened carotid artery, graded doses of adenosine evoked graded increases in NO output measured with a NO sensor that were greater in mature and middle-aged than juvenile rats. Infusion of adenosine to reduce mean arterial pressure (ABP) to ∼60 mmHg increased carotid vascular conductance (CVC) in all groups, but the increase was larger in mature rats; carotid blood flow (CBF) was unchanged in juvenile, increased in mature, but fell in 4/8 middle-aged rats. The NO synthase inhibitor nitro l-arginine methyl ester (l-NAME; 10 mg/kg iv) increased baseline ABP in all groups but caused larger percentage reductions in baseline CVC and CBF in mature and middle-aged than juvenile rats. Thereafter, the adenosine-evoked increase in CVC was unchanged in juvenile and middle-aged rats, yet CBF remained constant in juvenile but increased in middle-aged rats. In mature rats, the evoked increases in CVC and CBF were attenuated and further attenuated by l-NAME at 30 mg/kg. We propose that the ability of adenosine to release NO and cause vasodilation in the carotid artery and its circulation is greater in mature, than juvenile or middle-aged rats, but NO has greater tonic dilator influence in carotid circulation of mature and middle-aged than juvenile rats. By middle age, the lower limit of cerebral autoregulation has increased such that the tonic dilator influence of NO on ABP and CVC limits autoregulation of CBF to depressor responses. However, partial NO synthase inhibition overcomes this impairment, raising baseline ABP and allowing adenosine-evoked increases in CVC to increase CBF.

Nitric oxide mediates human chorionic gonadotrophin-induced prostaglandin E generation in rat oocyte - cumulus complexes

1997 ◽  
Vol 9 (4) ◽  
pp. 391 ◽  
Author(s):  
Alicia Jawerbaum ◽  
Elida T. Gonzalez ◽  
Alicia Faletti ◽  
Virginia Novaro ◽  
Martha A. F. Gimeno
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
No Synthase ◽  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Prostaglandin E ◽  
No Donors ◽  
Nos Inhibitors ◽  
Preovulatory Follicles

To determine whether nitric oxide (NO) generation mediates human chorionic gonadotrophin (hCG)-induced prostaglandin E (PGE) secretion by oocyte–cumulus complexes (OCC), the secretion of PGE by cultured rat OCC in the presence of NO donors and NO synthase (NOS) inhibitors was characterized. NO donors (sodium nitroprusside and 3-morpholino-sydnonimine- hydrochloride) increased PGE accumulation in OCC to values similar to those obtained in the presence of hCG. The three NOS inhibitors tested (N G -nitro-L-arginine methyl ester, NG -monomethyl-L-arginine and aminoguanidine) prevented the hCG-induced PGE accumulation in cultured OCC. This effect appears to be specific since D-enantiomers NG -nitro-D-arginine methyl ester and NG -monomethyl-D-arginine had no effect. The present results suggest that NO mediates the hCG-induced accumulation of PGE in rat OCC, a process which may occur in vivo in preovulatory follicles prior to ovulation.

Role of nitric oxide in regulation of vascular resistance in postnatal intestine

1995 ◽  
Vol 268 (6) ◽  
pp. G949-G958 ◽  
Author(s):  
C. A. Nankervis ◽  
P. T. Nowicki
Keyword(s):  
Nitric Oxide ◽  
Vascular Resistance ◽  
Age Groups ◽  
Calcium Ionophore ◽  
Similar Extent ◽  
Vascular Effects ◽  
A 23187

Studies were conducted to determine whether endothelial production of nitric oxide (NO) participates in the regulation of vascular resistance in postnatal swine intestine. In vivo, intra-arterial infusion of the arginine analogue NG-monomethyl-L-arginine (L-NMMA, 10(-4) M) increased intestinal vascular resistance 34% in 3-day-old animals and 9% in 35-day-old animals (P < 0.01); similar findings were noted during infusion of 10(-3) M L-NMMA. Mechanical augmentation of gut flow rate induced intestinal vasodilation in both age groups; L-NMMA eliminated this flow-induced dilation in intestine of 3- but not 35-day-old animals. In vitro, precontracted mesenteric artery rings from both age groups relaxed to a similar extent in response to the endothelium-independent nitrovasodilator sodium nitroprusside (SNP) and the calcium ionophore A-23187; the effect of A-23187, but not SNP, was eliminated by mechanical disruption of the endothelium. Acetylcholine (ACh) and substance P (SP), agents with vascular effects that are secondary to receptor-mediated activation of NO, caused greater relaxation of rings from younger than from older animals, and this effect was attenuated by L-NMMA or methylene blue. Unstimulated accumulation of guanosine 3',5'-cyclic monophosphate (cGMP) occurred to a similar extent in vessel segments from both groups. ACh and SP increased cGMP accumulation in segments from 3- but not from 35-day-old animals. We conclude that the NO-cGMP axis participates to a greater extent in regulation of intestinal vascular resistance in 3- than in 35-day-old swine.

scholarly journals Pyrogen–prostaglandin coupling in the pathogenesis of fever: evidence against a role for nitric oxide

1995 ◽  
Vol 73 (10) ◽  
pp. 1466-1474 ◽  
Author(s):  
Jane Redford ◽  
Isis Bishai ◽  
Flavio Coceani
Keyword(s):  
Nitric Oxide ◽  
Brain Tissue ◽  
Cyclic Gmp ◽  
Interleukin 1 ◽  
Prostaglandin E ◽  
Signal Transducer ◽  
Cerebral Tissue ◽  
Cerebral Microvessels

There is much debate on the mechanism by which blood-borne pyrogens trigger prostaglandin E2 (PGE2) synthesis in brain and fever. This investigation was undertaken to determine whether nitric oxide qualifies as a signal transducer for pyrogens at the interface between blood and brain. Experiments were carried out in vitro and in vivo using, respectively, preparations of cerebral tissue and microvessels from the rat, and the conscious, chronically instrumented cat. In vitro preparations produced PGE2 and its production increased during a 30-min treatment with interleukin 1 (brain tissue) or endotoxin (microvessels). In addition, both pyrogens increased cyclic GMP levels in cerebral microvessels. In both brain tissue and microvessels, NG-nitro-L-arginine had no effect on basal PGE2 release, while it curtailed the pyrogen-stimulated release. The same treatment reduced the cyclic GMP accumulation brought about by pyrogens in the microvessels. Conversely, in the conscious cat, inhibitors of nitric oxide synthesis (NG-monomethyl-L-argimne, NG-nitro-L-arginine) had no effect on fever and the concomitant elevation of PGE2 in cerebrospinal fluid, regardless of the pyrogen used (endotoxin, interleukin 1) and the route of administration (intravenous, intracerebroventricular). We conclude that nitric oxide may serve as a pyrogen mediator in brain. This mediator function, however, is seemingly not important in the development of fever.Key words: pyrogen, fever mechanism, nitric oxide, prostaglandin E2, blood–brain barrier.

scholarly journals Antibacterial and Anti-Inflammatory Activities ofPhysalis Alkekengivar.franchetiiand Its Main Constituents

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Zunpeng Shu ◽  
Na Xing ◽  
Qiuhong Wang ◽  
Xinli Li ◽  
Bingqing Xu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nuclear Translocation ◽  
Interleukin 1 ◽  
Inflammatory Activity ◽  
Prostaglandin E ◽  
Active Components ◽  
Necrosis Factor Alpha ◽  
Anti Inflammatory

This study was designed to determine whether the 50% EtOH fraction from AB-8 macroporous resin fractionation of a 70% EtOH extract ofP. Alkekengi(50-EFP) has antibacterial and/or anti-inflammatory activity bothin vivoandin vitroand to investigate the mechanism of 50-EFP anti-inflammatory activity. Additionally, this study sought to define the chemical composition of 50-EFP. Results indicated that 50-EFP showed significant antibacterial activityin vitroand efficacyin vivo. Moreover, 50-EFP significantly reduced nitric oxide (NO), prostaglandin E2(PGE2), tumor necrosis factor alpha (TNF-α), interleukin 1 (IL-1), and interleukin 6 (IL-6) production in lipopolysaccharide- (LPS-) stimulated THP-1 cells. Nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) (examined at the protein level) in THP-1 cells were suppressed by 50-EFP, which inhibited nuclear translocation of p65. Consistent with this anti-inflammatory activityin vitro, 50-EFP reduced inflammation in both animal models. Finally, seventeen compounds (8 physalins and 9 flavones) were isolated as major components of 50-EFP. Our data demonstrate that 50-EFP has antibacterial and anti-inflammatory activities bothin vitroandin vivo. The anti-inflammatory effect appears to occur, at least in part, through the inhibition of nuclear translocation of p65. Moreover, physalins and flavones are probably the active components in 50-EFP that exert antibacterial and anti-inflammatory activities.

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.

scholarly journals Increased lethality and defective pulmonary clearance of Streptococcus pneumoniae in microsomal prostaglandin E synthase-1-knockout mice

2016 ◽  
Vol 310 (11) ◽  
pp. L1111-L1120 ◽  
Author(s):  
Jennifer M. Dolan ◽  
Jason B. Weinberg ◽  
Edmund O'Brien ◽  
Anya Abashian ◽  
Megan C. Procario ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Streptococcus Pneumoniae ◽  
Host Defense ◽  
Bacterial Pneumonia ◽  
Bacterial Infections ◽  
Pneumococcal Pneumonia ◽  
Prostaglandin E ◽  
Prostaglandin E Synthase

The production of prostaglandin E2 (PGE2) increases dramatically during pneumococcal pneumonia, and this lipid mediator impairs alveolar macrophage (AM)-mediated innate immune responses. Microsomal prostaglandin E synthase-1 (mPGES-1) is a key enzyme involved in the synthesis of PGE2, and its expression is enhanced during bacterial infections. Genetic deletion of mPGES-1 in mice results in diminished PGE2 production and elevated levels of other prostaglandins after infection. Since PGE2 plays an important immunoregulatory role during bacterial pneumonia we assessed the impact of mPGES-1 deletion in the host defense against pneumococcal pneumonia in vivo and in AMs in vitro. Wild-type (WT) and mPGES-1 knockout (KO) mice were challenged with Streptococcus pneumoniae via the intratracheal route. Compared with WT animals, we observed reduced survival and increased lung and spleen bacterial burdens in mPGES-1 KO mice 24 and 48 h after S. pneumoniae infection. While we found modest differences between WT and mPGES-1 KO mice in pulmonary cytokines, AMs from mPGES-1 KO mice exhibited defective killing of ingested bacteria in vitro that was associated with diminished inducible nitric oxide synthase expression and reduced nitric oxide (NO) synthesis. Treatment of AMs from mPGES-1 KO mice with an NO donor restored bacterial killing in vitro. These results suggest that mPGES-1 plays a critical role in bacterial pneumonia and that genetic ablation of this enzyme results in diminished pulmonary host defense in vivo and in vitro. These results suggest that specific inhibition of PGE2 synthesis by targeting mPGES-1 may weaken host defense against bacterial infections.

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