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[PMID]: 28455132
[Au] Autor:Boonprom P; Boonla O; Chayaburakul K; Welbat JU; Pannangpetch P; Kukongviriyapan U; Kukongviriyapan V; Pakdeechote P; Prachaney P
[Ad] Address:Department of Anatomy, Faculty of Medicine, Khon Kaen University, Khon Kaen 40002, Thailand.
[Ti] Title:Garcinia mangostana pericarp extract protects against oxidative stress and cardiovascular remodeling via suppression of p47 and iNOS in nitric oxide deficient rats.
[So] Source:Ann Anat;212:27-36, 2017 Jul.
[Is] ISSN:1618-0402
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:N -Nitro-l-arginine methyl ester (l-NAME)-induced hypertension and cardiovascular remodeling are associated with oxidative stress and inflammation. Garcinia mangostana Linn., has been reported to have antioxidant and anti-inflammatory properties. This study investigated whether G. mangostana pericarp extract (GME) could prevent l-NAME-induced hemodynamic alterations, cardiovascular remodeling, oxidative stress and inflammation in rats. Male Sprague-Dawley rats were given 40mg/kg/day of l-NAME in drinking water to induce hypertension, and were simultaneously treated with GME at a dose of 200mg/kg/day. Rats that received l-NAME for five weeks had high blood pressure, left ventricular hypertrophy and thickening of aortic wall. Vascular superoxide production, plasma malondialdehyde (MDA), and plasma tumor necrosis factor alpha (TNF-α) were significantly increased in l-NAME-hypertensive rats (p<0.05). This was consistent with up-regulation of the p47 NADPH oxidase subunit and iNOS protein expression in aortic tissues (p<0.05). Low levels of plasma nitric oxide metabolites were observed in l-NAME hypertension. GME prevented the development of hypertension and cardiovascular remodeling induced by l-NAME with reduced oxidative stress and inflammation. These data suggest that GME had a protective effect against l-NAME-induced hypertension and cardiovascular remodeling via suppressing p47 NADPH oxidase subunit and iNOS protein expression resulting in enhancing NO bioavailability.
[Mh] MeSH terms primary: Cardiovascular System/drug effects
Garcinia mangostana/chemistry
Hypertension/drug therapy
Oxidative Stress/drug effects
Plant Extracts/pharmacology
[Mh] MeSH terms secundary: Animals
Antioxidants/metabolism
Antioxidants/pharmacology
Enzyme Inhibitors/administration & dosage
Enzyme Inhibitors/adverse effects
Free Radical Scavengers/metabolism
Fruit/chemistry
Hypertension/chemically induced
Hypertension/complications
Hypertension/metabolism
Hypertrophy, Left Ventricular/chemically induced
Hypertrophy, Left Ventricular/etiology
Hypertrophy, Left Ventricular/prevention & control
Inflammation/etiology
Male
Mesenteric Arteries/drug effects
Mesenteric Arteries/pathology
NADPH Oxidases/antagonists & inhibitors
NADPH Oxidases/metabolism
NG-Nitroarginine Methyl Ester/administration & dosage
NG-Nitroarginine Methyl Ester/adverse effects
Nitric Oxide/metabolism
Nitric Oxide Synthase Type II/antagonists & inhibitors
Plant Extracts/therapeutic use
Random Allocation
Rats
Rats, Sprague-Dawley
Ventricular Remodeling/drug effects
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Antioxidants); 0 (Enzyme Inhibitors); 0 (Free Radical Scavengers); 0 (Plant Extracts); 31C4KY9ESH (Nitric Oxide); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.6.3.- (NADPH Oxidases); EC 1.6.3.1 (neutrophil cytosolic factor 1); V55S2QJN2X (NG-Nitroarginine Methyl Ester)
[Em] Entry month:1801
[Cu] Class update date: 180130
[Lr] Last revision date:180130
[Js] Journal subset:IM
[Da] Date of entry for processing:170430
[St] Status:MEDLINE

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[PMID]: 29243902
[Au] Autor:Tyurenkov IN; Perfilova VN; Lashhenova LI; Zhakupova GA; Lebedeva SA
[Ti] Title:Comparison of physical development and rate of formation sensory-motor reflexes offspring of rats with different experimental model of preeclampsia.
[So] Source:Patol Fiziol Eksp Ter;60(3):10-7, 2016 Jul-Sep.
[Is] ISSN:0031-2991
[Cp] Country of publication:Russia (Federation)
[La] Language:eng
[Ab] Abstract:Summary: A comparative study of the physical development and the rate of formation of sensory-motor reflexes offspring of rats with experimental preeclampsia (EP) was carried out. In the first experimental group EP was modeled intraperitoneal conduct of L-NAME at a dose of 25 mg/kg from 14 to 21 days of gestation, the second experimental group - the replacement of drinking water by 1.8% sodium chloride solution for the entire period of gestation. In the offspring of both groups, there was a delay of physical development, which was reflected in the later timing of the hair coat development, incisor eruption, pinna detachment as compared to the pups in the control group. It also noted the gap in the formation of sensory-motor reflexes and vestibular reactions. This was manifested in the delayed appearance of the olfactory response, auditory sensitivity, later performing tests «righting reflex¼, «negative geotaxis¼, «aerial righting reflex¼, «cliff avoidance¼, «horizontal wire test¼, «raising the head and forelegs¼, «supporting their bodies on hind legs¼ as compared to the indices of the pups of the female rats with an uncomplicated pregnancy. The most pronounced lag in postnatal development was observed in the offspring of rats with EP, which instead of drinking water was prepared 1.8% sodium chloride during the entire period of gestation. The purpose: To make a comparative study of the impact of ADMA-like preeclampsia (PE) and preeclampsia modeled by the replacement of drinking water consumed by female rats during gestation with 1.8% NaCl solution on the physical development and the rate of the maturation of sensory motor reflexes of their offspring. Methods: The study was performed on three groups of pregnant female rats aged 3-4 months whose original weight was 210-250 g and their pups. They were divided into three groups: 1: Control group including female rats with an uncomplicated pregnancy (n = 6) and their pups (n = 49); 2. Experimental group 1 - pregnant female rats with PE (n = 6) induced by intraabdominal introduction of L-NAME at a dose of 25 mg/kg from 14 to 21 day of gestation (ADMA-like preeclampsia) and their offspring (n = 35); 3. Experimental group 2 - pregnant female rats with PE (n = 6) modeled by the replacement of drinking throughout gestation with 1.8% NaCl solution and their pups. When studying the physical development of the pups we considered the terms of pinna detachment, hair coat development, incisor eruption and the time when they began to open their eyes. To estimate the rate of the maturation of sensory motor reflexes and motor coordination of the pups of the rats with PE we analyzed the time when they started to support their bodies on hind legs, lift their bodies off the floor, crawl, raise their head and forelegs, show the aerial righting reflex and the righting reflex, negative geotaxis, reactions to auditory and olfactory stimuli as well as the time they managed to stay on the horizontal wire. Results: The pups of the female rats with PE of both experimental groups were found to have later pinna detachment, incisor eruption and hair coat development as compared to the indices of the control group. In addition, the offspring of the experimental groups demonstrated a delay in the performance of the following tests: «righting reflex¼, «negative geotaxis¼, «aerial righting reflex¼, «cliff avoidance¼, «horizontal wire test¼, «raising the head and forelegs¼, «supporting their bodies on hind legs¼, «reaction to an olfactory stimulus¼ and «reaction to an auditory stimulus¼ as compared to the indices of the pups of the female rats with an uncomplicated pregnancy. Conclusion: PE induced by the introduction of ADMA to pregnant female rats and by the replacement of drinking water consumed by female rats during gestation with 1.8% NaCl solution causes a delay in physical development, maturation of sensory motor reflexes and vestibular reactions in their offspring.
[Mh] MeSH terms primary: NG-Nitroarginine Methyl Ester/adverse effects
Pre-Eclampsia/chemically induced
Prenatal Exposure Delayed Effects/physiopathology
Reflex, Abnormal/drug effects
Sensorimotor Cortex/physiopathology
[Mh] MeSH terms secundary: Animals
Female
NG-Nitroarginine Methyl Ester/pharmacology
Pre-Eclampsia/metabolism
Pre-Eclampsia/physiopathology
Pregnancy
Prenatal Exposure Delayed Effects/chemically induced
Prenatal Exposure Delayed Effects/pathology
Rats
Sensorimotor Cortex/pathology
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:V55S2QJN2X (NG-Nitroarginine Methyl Ester)
[Em] Entry month:1801
[Cu] Class update date: 180118
[Lr] Last revision date:180118
[Js] Journal subset:IM
[Da] Date of entry for processing:171216
[St] Status:MEDLINE

  3 / 11970 MEDLINE  
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[PMID]: 29212068
[Au] Autor:Kitay AM; Link A; Geibel JP
[Ad] Address:Department of Surgery, Yale University, School of Medicine, New Haven, Connecticut, USA.
[Ti] Title:Activation of Secretagogue Independent Gastric Acid Secretion via Endothelial Nitric Oxide Synthase Stimulation in Rats.
[So] Source:Cell Physiol Biochem;44(4):1606-1615, 2017.
[Is] ISSN:1421-9778
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:BACKGROUND/AIMS: L-arginine is an important mediator of cell division, wound healing, and immune function. It can be transformed by the nitric oxide synthase (NOS) to nitric oxide (NO), an important cell signaling molecule. Recent studies from our laboratory demonstrate specific effects of L-arginine (10mM) exposure on gastric acid secretion in rat parietal cells. METHODS: Studies were performed with isolated gastric glands and the pH sensitive dye BCECF-AM +/- L-arginine to examine its effects on acid secretion. The direct NO-donor diethylamine NONOate sodium salt hydrate, was also used while monitoring intracellular pH. The specific inhibitor of the intracellular NO signal cascade ODQ was also used. RESULTS: We found that gastric proton extrusion was activated with application of L-arginine (10mM), in a separate series when L-arginine (10mM) + L-NAME (30µM) were added there was no acid secretion. Addition of the NO-donor diethylamine NONOate sodium salt hydrate (10µM) also induced acid secretion. When the selective sGC-inhibitor ODQ was added with NONOate we did not observe acid secretion. CONCLUSION: We conclude that L-arginine is a novel secretagogue, which can mediate gastric acid secretion. Furthermore, the intake of L-arginine causes direct activation of the H+, K+ ATPase and increased proton extrusion from parietal cells resulting in the increased risk for acid-related diseases. The NO/sGC/cGMP pathway has never been described as a possible intracellular mechanism for H+, K+ ATPase activation before and presents a completely new scientific finding. Moreover, our studies demonstrate a novel role for L-NAME to effectively eliminate NOS induced acid secretion and thereby reducing the risk for L-arginine inducible ulcer disease.
[Mh] MeSH terms primary: Gastric Acid/secretion
Nitric Oxide Synthase Type III/metabolism
[Mh] MeSH terms secundary: Animals
Arginine/pharmacology
H(+)-K(+)-Exchanging ATPase/metabolism
Hydrogen-Ion Concentration
Male
NG-Nitroarginine Methyl Ester/pharmacology
Oxadiazoles/pharmacology
Parietal Cells, Gastric/cytology
Parietal Cells, Gastric/drug effects
Parietal Cells, Gastric/metabolism
Quinoxalines/pharmacology
Rats
Rats, Sprague-Dawley
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one); 0 (Oxadiazoles); 0 (Quinoxalines); 94ZLA3W45F (Arginine); EC 1.14.13.39 (Nitric Oxide Synthase Type III); EC 3.6.3.10 (H(+)-K(+)-Exchanging ATPase); V55S2QJN2X (NG-Nitroarginine Methyl Ester)
[Em] Entry month:1801
[Cu] Class update date: 180118
[Lr] Last revision date:180118
[Js] Journal subset:IM
[Da] Date of entry for processing:171207
[St] Status:MEDLINE
[do] DOI:10.1159/000485755

  4 / 11970 MEDLINE  
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[PMID]: 28466812
[Au] Autor:Ovali MA; Uzun M
[Ad] Address:Department of Physiology, Faculty of Medicine, Çanakkale Onsekiz Mart University, Çanakkale 17100,Turkey.
[Ti] Title:The effects of melatonin administration on KCNQ and KCNH2 gene expressions and QTc interval in pinealectomised rats.
[So] Source:Cell Mol Biol (Noisy-le-grand);63(3):45-50, 2017 03 31.
[Is] ISSN:1165-158X
[Cp] Country of publication:France
[La] Language:eng
[Ab] Abstract:Melatonin is a hormone secreted from the pineal gland and has different cardiovascular effects. KCNQ genes expressed in aorta related with vascu- lar tone and KCNH2 gene characterised in left ventricle associated with QT duration. The aim of this study was to investigate the effects of melatonin on the regulation of the blood pressure and the relationships between the expressions of aorta KCNQ1-5, left ventricle KCNH2 genes and the QTc interval. For that purpose, 42 male adult Sprague-Dawley rats were devided into six groups; SHAM, SHAM+L-NAME, PLT, PLT+L-NAME, PLT+MEL and PLT+L-NAME+MEL. Pinealectomy operation was applied in PLT groups. L-NAME was added in drinking water (40 mg/kg/day) and melatonin was given subcutanously (5 mg/kg/day). The blood pressure, heart rate (HR) and QTc interval values were recorded on 0, 1st, 7th, 14th and 21st days of experiment. Left ventricle and thoracic aorta samples were obtained to investigate the changes of gene expression levels of KCNQ1-5 and KCNH2, respectively. The increased blood pressure and HR were observed in SHAM+L-NAME, PLT, and PLT+L-NAME groups compared to MEL and SHAM groups (p<0.05). On the other hand, the long QTc interval was recorded in PLT and all L-NAME groups compared to others (p<0.05). The decreases in KCNH2 gene expression levels were observed in groups have QTc prolongation. In conclusion, PLT operation could cause an increasing in blood pressure, HR and QTc duration, melatonin was able to prevent these increasings and could change KCNQ and KCNH2 gene expresion profiles. Further molecular studies are required to evaluate these effects.
[Mh] MeSH terms primary: ERG1 Potassium Channel/metabolism
Electrocardiography
Gene Expression/drug effects
KCNQ Potassium Channels/metabolism
Melatonin/pharmacology
[Mh] MeSH terms secundary: Animals
Blood Pressure/drug effects
ERG1 Potassium Channel/genetics
Heart Rate/drug effects
Infusions, Subcutaneous
KCNQ Potassium Channels/genetics
Male
NG-Nitroarginine Methyl Ester/pharmacology
Pineal Gland/surgery
Rats
Rats, Sprague-Dawley
Real-Time Polymerase Chain Reaction
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (ERG1 Potassium Channel); 0 (KCNQ Potassium Channels); 0 (Kcnh2 protein, rat); JL5DK93RCL (Melatonin); V55S2QJN2X (NG-Nitroarginine Methyl Ester)
[Em] Entry month:1801
[Cu] Class update date: 180117
[Lr] Last revision date:180117
[Js] Journal subset:IM
[Da] Date of entry for processing:170504
[St] Status:MEDLINE
[do] DOI:10.14715/cmb/2017.63.3.9

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[PMID]: 29017485
[Au] Autor:Bilanda DC; Dzeufiet PDD; Kouakep L; Aboubakar BFO; Tedong L; Kamtchouing P; Dimo T
[Ad] Address:Department of Animal Biology and Physiology, Laboratory of Animal Physiology, University of Yaounde I, P.O. Box 812, Yaounde, Cameroon. bilandad@yahoo.comm.
[Ti] Title:Bidens pilosa Ethylene acetate extract can protect against L-NAME-induced hypertension on rats.
[So] Source:BMC Complement Altern Med;17(1):479, 2017 Oct 10.
[Is] ISSN:1472-6882
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Essential hypertension is mainly caused by endothelial dysfunction which results from nitric oxide (NO) deficiency. The present study was design to evaluate the protective effect of Bidens pilosa ethylene acetate extract (Bp) on L-NAME induced hypertension and oxidative stress in rats. METHODS: Male Wistar rats were used to induce hypertension by the administration of L-NAME (a non-pecific nitric oxide inhibitor) (50 mg/kg/day). The others groups were receiving concomitantly L-NAME plus Bp extract (75 and 150 mg/kg/day) or losartan (25 mg/kg/day). All the treatments were given orally for 4 weeks. At the end of the treatment, the hemodynamic parameters were recorded using the direct cannulation method. The effects of the extract on lipid profile, kidney and liver functions as well as oxidative stress markers were evaluated by colorimetric method. Results were expressed as the mean ± SEM. The difference between the groups was compared using one-way analysis of variance (ANOVA) followed by the Duncan's post hoc test. RESULTS: Animals receiving L-NAME presented high blood pressure, normal heart rate and lipid profile as well as NO depletion, liver and kidney injuries and oxidative stress. The concomitant treatment with L-NAME and Bp or losartan succeeded to prevent the raised of blood pressure and all the other injuries without affecting the heart rate. CONCLUSION: These results confirm the antihypertensive effects of Bidens pilosa and highlight its protective properties in L-NAME model of hypertension in rat, probably due to the presence of Quercetin 3,3 '-dimethyl ether 7-0-ß-D-glucopyranoside.
[Mh] MeSH terms primary: Bidens/chemistry
Hypertension/metabolism
Oxidative Stress/drug effects
Plant Extracts/pharmacology
Protective Agents/pharmacology
[Mh] MeSH terms secundary: Acetates
Animals
Ethylenes
Hypertension/prevention & control
Kidney/drug effects
Lipids
Liver/drug effects
NG-Nitroarginine Methyl Ester
Plant Extracts/chemistry
Protective Agents/chemistry
Rats, Wistar
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Acetates); 0 (Ethylenes); 0 (Lipids); 0 (Plant Extracts); 0 (Protective Agents); 91GW059KN7 (ethylene); V55S2QJN2X (NG-Nitroarginine Methyl Ester)
[Em] Entry month:1710
[Cu] Class update date: 171027
[Lr] Last revision date:171027
[Js] Journal subset:IM
[Da] Date of entry for processing:171012
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-017-1972-0

  6 / 11970 MEDLINE  
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[PMID]: 28973370
[Au] Autor:Song M; Wu J; Lei Y; Sun X
[Ad] Address:Department of Ophthalmology & Visual Science, Eye & ENT Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
[Ti] Title:Genetic Deletion of the NOS3 Gene in CAV1-/- Mice Restores Aqueous Humor Outflow Function.
[So] Source:Invest Ophthalmol Vis Sci;58(12):4976-4987, 2017 Oct 01.
[Is] ISSN:1552-5783
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Purpose: The purpose of this study was to investigate the impact of genetic deletion of NOS3 in CAV1-/- mice on aqueous humor outflow function using a mouse genetic double knockout model (DKO, NOS3-/- CAV1-/-). Methods: IOP was measured in DKO, NOS3 KO, CAV1 KO, and wild-type (WT) mice by rebound tonometry. Outflow facility was measured by perfusing enucleated mouse eyes at multiple pressure steps. Sodium nitroprusside (SNP) and L-NG-nitroarginine methyl ester (L-NAME) was administered topically, whereas the contralateral eyes served as vehicle controls. IOP was measured in both eyes before drug treatment and 1 hour after the last drug treatment. Mock aqueous humor ± the nitric oxide (NO) donor SNP or NOS inhibitor L-NAME was perfused into enucleated eyes. Results: IOP was 11 ± 0.23 mm Hg in DKO mice, which was similar to WT mice and significantly lower than CAV1 KO mice (n = 18, P > 0.05). NOS3 deletion in CAV1-/- mice resulted in a 1.9-fold increase in conventional outflow facility (Ccon) compared with CAV1 KO mice (n = 7, P < 0.05). Topical application of NO donor SNP did not significantly change IOP (n = 18, P > 0.05) or Ccon in DKO mice (SNP, n = 20; vehicle, n = 11, P > 0.05). Topical application of L-NAME significantly increased IOP in WT, DKO, and CAV1 mice by reducing Ccon. Nitrotyrosine and PKG levels of DKO mice were similar to, whereas sGC was lower than, WT mice (P < 0.05). Conclusions: Genetic deletion of NOS3 in CAV1-deficient mice restored IOP and conventional aqueous humor drainage to WT level. NOS3 and CAV1 interaction is important to IOP regulation.
[Mh] MeSH terms primary: Aqueous Humor/physiology
Caveolin 1/deficiency
Gene Deletion
Nitric Oxide Synthase Type III/physiology
[Mh] MeSH terms secundary: Animals
Aqueous Humor/drug effects
Disease Models, Animal
Enzyme Inhibitors/pharmacology
Intraocular Pressure/drug effects
Mice
Mice, Knockout
NG-Nitroarginine Methyl Ester/pharmacology
Nitric Oxide Donors/pharmacology
Nitric Oxide Synthase Type III/genetics
Nitroprusside/pharmacology
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Caveolin 1); 0 (Enzyme Inhibitors); 0 (Nitric Oxide Donors); 169D1260KM (Nitroprusside); EC 1.14.13.39 (NOS3 protein, human); EC 1.14.13.39 (Nitric Oxide Synthase Type III); V55S2QJN2X (NG-Nitroarginine Methyl Ester)
[Em] Entry month:1710
[Cu] Class update date: 171006
[Lr] Last revision date:171006
[Js] Journal subset:IM
[Da] Date of entry for processing:171004
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.16-21072

  7 / 11970 MEDLINE  
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[PMID]: 28966136
[Au] Autor:Raheja R; Gupta H; Pandey U; Deshpande SB
[Ad] Address:Department of Physiology, Institute of Medical Sciences, Banaras Hindu University, Varanasi 221005, India.
[Ti] Title:Lignocaine augments the in-vitro uterine contractions involving NO-guanylyl cyclase dependent mechanisms.
[So] Source:Life Sci;190:52-57, 2017 Dec 01.
[Is] ISSN:1879-0631
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:AIMS: Lignocaine is used during intrapartum and postpartum period but there are conflicting reports regarding the effect of lignocaine on uterine contractility. Therefore, this study was undertaken to delineate the effect of lignocaine on uterine contractility and the underlying mechanisms. MAIN METHODS: The in vitro contractions were recorded from the uterine segments obtained from adult rats (in estrous phase) and also from human myometrial tissue. Effect of lignocaine on spontaneous uterine contractions was recorded in the absence or presence of antagonists. Effect of sodium nitroprusside (SNP, NO donor) on uterine contractility was assessed. The NO was assayed (indicator of NO activity) from the supernatant after exposing the myometrial tissue to lignocaine in the absence or the presence of L-NAME or hemoglobin. KEY FINDINGS: Lignocaine (100µM) increased the amplitude of uterine contractions by 75% with no alterations in frequency. Similar magnitude of increase was seen with human myometrial tissue also. The spontaneous activities were absent in Ca -free or in nifedipine (10µM) containing medium. Heparin (IP blocker, 10IU/ml), but not the indomethacin (10µM) blocked the lignocaine-induced augmentation. L-NAME (NOS inhibitor, 10µM) or methylene blue (guanylyl cyclase inhibitor, 100µM) partially blocked the lignocaine-induced augmentation. SNP (30µM) increased the amplitude of spontaneous uterine contractions. Lignocaine increased the NO content (indicator of NO activity) of uterine tissue and the increase was blocked by L-NAME or hemoglobin. SIGNIFICANCE: Present observations indicate that lignocaine augments the amplitude of uterine contractions via Ca -dependent mechanisms involving NO-G cyclase-dependent mechanisms.
[Mh] MeSH terms primary: Anesthetics, Local/pharmacology
Guanylate Cyclase/metabolism
Lidocaine/pharmacology
Nitric Oxide/metabolism
Uterine Contraction/drug effects
[Mh] MeSH terms secundary: Animals
Calcium/metabolism
Female
Hemoglobins/metabolism
Humans
NG-Nitroarginine Methyl Ester/pharmacology
Nifedipine/pharmacology
Nitroprusside/pharmacology
Rats
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Anesthetics, Local); 0 (Hemoglobins); 169D1260KM (Nitroprusside); 31C4KY9ESH (Nitric Oxide); 98PI200987 (Lidocaine); EC 4.6.1.2 (Guanylate Cyclase); I9ZF7L6G2L (Nifedipine); SY7Q814VUP (Calcium); V55S2QJN2X (NG-Nitroarginine Methyl Ester)
[Em] Entry month:1710
[Cu] Class update date: 171030
[Lr] Last revision date:171030
[Js] Journal subset:IM
[Da] Date of entry for processing:171003
[St] Status:MEDLINE

  8 / 11970 MEDLINE  
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[PMID]: 28864378
[Au] Autor:Shamardl HA; El-Ashmony SM; Kamel HF; Fatani SH
[Ad] Address:Department of Pharmacology (HAS), Faculty of Medicine, Fayoum University, Fayoum, Egypt; Department of Pharmacology & Clinical Pharmacy (SME), Faculty of Pharmacy, Umm Al-Qura University, Makkah, Saudi Arabia. Electronic address: hanan2remember@yahoo.com.
[Ti] Title:Potential Cardiovascular and Renal Protective Effects of Vitamin D and Coenzyme Q in l-NAME-Induced Hypertensive Rats.
[So] Source:Am J Med Sci;354(2):190-198, 2017 Aug.
[Is] ISSN:1538-2990
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Hypertension is one of the primary modifiable risk factors for cardiovascular disease. Adequate vitamin D (vit D) levels have been shown to reduce vascular smooth muscle contraction and to increase arterial compliance, which may be beneficial in hypertension. Further, coenzyme Q10 (COQ10) through its action to lower oxidative stress has been reported to have beneficial effects on hypertension and heart failure. This study examined the possible cardiac and renal protective effects of vit D and COQ10 both separately and in combination with an angiotensin II receptor blocker, valsartan (vals) in l-NAME hypertensive rats. MATERIALS AND METHODS: Hypertension was induced in rats by l-NAME administration. Following induction of hypertension, the rats were assigned into the following 6 subgroups: an l-NAME alone group and treated groups receiving the following drugs intraperitoneally for 6 weeks; vals, vit D, COQ10 and combination of vals with either vit D or COQ10. A group of normotensive rats were used as negative controls. At the end of the treatment period, blood pressure, serum creatinine, blood urea nitrogen, lipids and serum, cardiac and renal parameters of oxidative stress were measured. RESULTS: Compared to the l-NAME only group, all treatments lowered systolic, diastolic, mean arterial pressure, total cholesterol, low-density lipoprotein cholesterol, and creatinine levels as well as TNF-α and malondialdehyde. Further, the agents increased serum, cardiac and renal total antioxidant capacity. Interestingly, the combination of agents had further effects on all the parameters compared to treatment with each single agent. CONCLUSIONS: The study suggests that the additive protective effects of vit D and COQ10 when used alone or concurrent with vals treatment in hypertensive rats may be due to their effects as antioxidants, anticytokines and blood pressure conservers.
[Mh] MeSH terms primary: Hypertension/drug therapy
Ubiquinone/analogs & derivatives
Valsartan/pharmacology
Vitamin D/pharmacology
[Mh] MeSH terms secundary: Angiotensin II Type 1 Receptor Blockers/pharmacology
Animals
Cardiovascular Diseases/drug therapy
Hypertension/chemically induced
Kidney Diseases/drug therapy
NG-Nitroarginine Methyl Ester/toxicity
Rats
Rats, Wistar
Ubiquinone/pharmacology
Ubiquinone/therapeutic use
Vitamin D/therapeutic use
Vitamins/pharmacology
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Angiotensin II Type 1 Receptor Blockers); 0 (Vitamins); 1339-63-5 (Ubiquinone); 1406-16-2 (Vitamin D); 80M03YXJ7I (Valsartan); EJ27X76M46 (coenzyme Q10); V55S2QJN2X (NG-Nitroarginine Methyl Ester)
[Em] Entry month:1709
[Cu] Class update date: 170908
[Lr] Last revision date:170908
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:170903
[St] Status:MEDLINE

  9 / 11970 MEDLINE  
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[PMID]: 28781258
[Au] Autor:Medvedev DV; Zvyagina VI; Uryasev OM; Belskikh ES; Bulatetskiy SV; Ryabkov AN
[Ad] Address:Ryazan State Medical University.
[Ti] Title:Metabolicheskie izmeneniia v mitokhondriiakh legkikh pri éksperimental'noi gipergomotsisteinemii u krys. [Metabolic changes in pulmonary mitochondria of rats with experimental hyperhomocysteinemia].
[So] Source:Biomed Khim;63(3):248-254, 2017 May.
[Is] ISSN:2310-6972
[Cp] Country of publication:Russia (Federation)
[La] Language:rus
[Ab] Abstract:Hyperhomocysteinemia is a risk factor for many human diseases, including pulmonary pathologies. In this context much interest attracts secondary mitochondrial dysfunction, which is an important link in pathogenesis of diseases associated with hyperhomocysteinemia. The study was conducted using male Wistar rats. It was found that under conditions of severe hyperhomocysteinemia caused by administration of methionine, homocysteine was accumulated in lung mitochondria thus suggesting a direct toxic effect on these organelles. However, we have not observed any significant changes in the activity of mitochondrial enzymes involved in tissue respiration (succinate dehydrogenase) and oxidative phosphorylation (H+-ATPase) and of cytoplasmic lactate dehydrogenase. Also there was no accumulation of lactic acid in the cytoplasm. Animals with severe hyperhomocysteinemia had higher levels of lung mitochondrial protein carbonylation, decreased reserve-adaptive capacity, and increased superoxide dismutase activity. These results indicate that severe hyperhomocysteinemia causes development of oxidative stress in lung mitochondria, which is compensated by activation of antioxidant protection. These changes were accompanied by a decrease in the concentration of mitochondrial nitric oxide metabolites. Introduction to animals a nonselective NO-synthase inhibitor L-NAME caused similar enhancement of mitochondrial protein carbonylation. It demonstrates importance of reducing bioavailability of nitric oxide, which is an antioxidant in physiological concentrations, in the development of oxidative stress in lung mitochondria during hyperhomocysteinemia. Key words: hyperhomocysteinemia, nitric oxide, lung, oxidative stress, mitochondria.
[Mh] MeSH terms primary: Homocysteine/metabolism
Hyperhomocysteinemia/metabolism
Lung/metabolism
Methionine/adverse effects
Mitochondria/drug effects
[Mh] MeSH terms secundary: Animals
Enzyme Inhibitors/pharmacology
Homocysteine/agonists
Humans
Hyperhomocysteinemia/chemically induced
Hyperhomocysteinemia/pathology
L-Lactate Dehydrogenase/metabolism
Lung/drug effects
Lung/pathology
Male
Methionine/administration & dosage
Mitochondria/metabolism
Mitochondrial Proton-Translocating ATPases/metabolism
NG-Nitroarginine Methyl Ester/pharmacology
Nitric Oxide/metabolism
Oxidative Phosphorylation
Oxidative Stress/drug effects
Protein Carbonylation/drug effects
Rats
Rats, Wistar
Succinate Dehydrogenase/metabolism
Superoxide Dismutase/metabolism
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Enzyme Inhibitors); 0LVT1QZ0BA (Homocysteine); 31C4KY9ESH (Nitric Oxide); AE28F7PNPL (Methionine); EC 1.1.1.27 (L-Lactate Dehydrogenase); EC 1.15.1.1 (Superoxide Dismutase); EC 1.3.99.1 (Succinate Dehydrogenase); EC 3.6.3.- (Mitochondrial Proton-Translocating ATPases); V55S2QJN2X (NG-Nitroarginine Methyl Ester)
[Em] Entry month:1709
[Cu] Class update date: 170912
[Lr] Last revision date:170912
[Js] Journal subset:IM
[Da] Date of entry for processing:170808
[St] Status:MEDLINE
[do] DOI:10.18097/PBMC20176303248

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[PMID]: 28778917
[Au] Autor:Trujillo AN; Katnik C; Cuevas J; Cha BJ; Taylor-Clark TE; Breslin JW
[Ad] Address:Department of Molecular Pharmacology and Physiology, Morsani College of Medicine, University of South Florida, Tampa, Florida.
[Ti] Title:Modulation of mesenteric collecting lymphatic contractions by σ -receptor activation and nitric oxide production.
[So] Source:Am J Physiol Heart Circ Physiol;313(4):H839-H853, 2017 Oct 01.
[Is] ISSN:1522-1539
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Recently, it has been reported that a σ-receptor antagonist could reduce inflammation-induced edema. Lymphatic vessels play an essential role in removing excess interstitial fluid. We tested the hypothesis that activation of σ-receptors would reduce or weaken collecting lymphatic contractions. We used isolated, cannulated rat mesenteric collecting lymphatic vessels to study contractions in response to the σ-receptor agonist afobazole in the absence and presence of different σ-receptor antagonists. We used RT-PCR and Western blot analysis to investigate whether these vessels express the σ -receptor and immunofluorescence confocal microscopy to examine localization of the σ -receptor in the collecting lymphatic wall. Using -nitro-l-arginine methyl ester (l-NAME) pretreatment before afobazole in isolated lymphatics, we tested the role of nitric oxide (NO) signaling. Finally, we used 4-amino-5-methylamino-2',7'-difluorofluorescein diacetate fluorescence as an indicator to test whether afobazole increases NO release in cultured lymphatic endothelial cells. Our results show that afobazole (50-150 µM) elevated end-systolic diameter and generally reduced pump efficiency and that this response could be partially blocked by the σ -receptor antagonists BD 1047 and BD 1063 but not by the σ -receptor antagonist SM-21. σ -Receptor mRNA and protein were detected in lysates from isolated rat mesenteric collecting lymphatics. Confocal images with anti-σ -receptor antibody labeling suggested localization in the lymphatic endothelium. Blockade of NO synthases with l-NAME inhibited the effects of afobazole. Finally, afobazole elicited increases in NO production from cultured lymphatic endothelial cells. Our findings suggest that the σ -receptor limits collecting lymphatic pumping through a NO-dependent mechanism. Relatively little is known about the mechanisms that govern contractions of lymphatic vessels. σ -Receptor activation has been shown to reduce the fractional pump flow of isolated rat mesenteric collecting lymphatics. The σ -receptor was localized mainly in the endothelium, and blockade of nitric oxide synthase inhibited the effects of afobazole.
[Mh] MeSH terms primary: Lymphatic Vessels/drug effects
Lymphatic Vessels/metabolism
Mesentery/drug effects
Mesentery/metabolism
Nitric Oxide/biosynthesis
Receptors, Opioid, delta/agonists
[Mh] MeSH terms secundary: Animals
Benzimidazoles/pharmacology
Cells, Cultured
Endothelial Cells/drug effects
Endothelial Cells/metabolism
Enzyme Inhibitors/pharmacology
Male
Morpholines/pharmacology
Muscle Contraction/drug effects
Muscle, Smooth, Vascular/drug effects
NG-Nitroarginine Methyl Ester/pharmacology
Rats
Rats, Sprague-Dawley
Receptors, Opioid, delta/antagonists & inhibitors
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (2-((2-morpholino)ethylthio)-5-ethoxybenzimidazole); 0 (Benzimidazoles); 0 (DOR1 protein, rat); 0 (Enzyme Inhibitors); 0 (Morpholines); 0 (Receptors, Opioid, delta); 31C4KY9ESH (Nitric Oxide); V55S2QJN2X (NG-Nitroarginine Methyl Ester)
[Em] Entry month:1710
[Cu] Class update date: 171108
[Lr] Last revision date:171108
[Js] Journal subset:IM
[Da] Date of entry for processing:170806
[St] Status:MEDLINE
[do] DOI:10.1152/ajpheart.00702.2016


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