Insulin-induced endothelin release and vasoreactivity in hypertriglyceridemic and hypertensive rats

1999 ◽  
Vol 277 (1) ◽  
pp. H399-H404 ◽  
Author(s):  
Pilar Nava ◽  
Verónica Guarner ◽  
Rosalinda Posadas ◽  
Israel Pérez ◽  
Guadalupe Baños
Keyword(s):  
Drinking Water ◽  
Receptor Antagonist ◽  
Wistar Rats ◽  
Receptor Blocker ◽  
Hypertensive Rats ◽  
Contractile Responses ◽  
Femoral Arteries ◽  
Male Wistar Rats

Insulin-elicited endothelin release in hypertriglyceridemic, hypertensive, hyperinsulinemic (HTG) rats was shown. Weanling male Wistar rats were given 30% sucrose in their drinking water for 20–24 wk. In vitro contractions of aorta and femoral arteries were elicited with 40 mM KCl. Endothelin release induced with KCl plus 50 μU/ml insulin resulted in increases in contractile responses: 41 ± 5.9 and 57 ± 6% for control and 65.5 ± 6 and 95 ± 9% for HTG aortas and femoral arteries, respectively. The endothelin ETB-receptor blocker BQ-788 decreased responses to KCl + insulin by 39 ± 8 and 53 ± 5% in control and 48 ± 13 and 79 ± 3.5% in HTG aortas and femoral arteries, respectively. The ETA-receptor antagonist PD-151242 inhibited these responses by 12 ± 10 and 1 ± 9% in control and by 51.5 ± 9 and 58.5 ± 1% in HTG aortas and femoral arteries, respectively. These results suggest that endothelin may contribute to the hypertension in this model.

Renal Cortical Slices: An In Vitro Model for Kidney Metabolism and Toxicity

1992 ◽  
Vol 20 (1) ◽  
pp. 71-76
Author(s):  
Andrea Trevisan ◽  
Stefano Maso ◽  
Paola Meneghetti
Keyword(s):  
Wistar Rats ◽  
Reduced Glutathione ◽  
Organic Anion ◽  
Cortical Slice ◽  
Lactate Dehydrogenase Release ◽  
Age Related ◽  
Renal Cortical Slice ◽  
Male Wistar Rats ◽  
Vitro Model

The in vitro renal cortical slice model was used to study: 1) the effects on the kidney of some haloalkanes and haloalkenes using 3-month-old male Wistar rats; 2) influence of age and sex on renal cortical slice indices in non-treated rats; and 3) effects of 1,2-dichloropropane on the slices after pretreatment of 3-month-old male Wistar rats with DL-butathionine-[S,R]-sulphoximine. The most nephrotoxic chemical used was 1,3-dichloropropene, which caused a total depletion in the levels of reduced glutathione, a high peroxidation of lipid (about three thousand-fold with respect to control), a significant release of tubular enzymes into the medium, and loss of organic anion ( p-aminohippurate) accumulation. All the chemicals affected the cytosol more than the brush border. The most remarkable age-related differences in the untreated slices were the progressive decrease of reduced glutathione (p<0.05 from three months of age), and an increase in lactate dehydrogenase release into the medium (p<0.05 from six months of age). By contrast, sex differences were slight. The ‘treatment with 1,2-dichloropropane of slices prepared from rats pretreated with DL-butathionine-[S,R]-sulphoximine significantly increased the depletion of glutathione content (p<0.05) and malondialdehyde release in the medium (p<0.001) caused by the solvent alone.

scholarly journals Haloperidol and Risperidone Induce Apoptosis Neuronal Cell : Invivo Study

2020 ◽  
Vol 1 (1) ◽  
Author(s):  
Ester G Panserga ◽  
Cecep S Kristanto ◽  
Budi Pratiti ◽  
Patricia Wulandari
Keyword(s):  
Cell Apoptosis ◽  
Wistar Rats ◽  
Caspase 3 ◽  
Neuronal Cells ◽  
Neuronal Cell ◽  
Total Percentage ◽  
White Rats ◽  
Male Wistar Rats ◽  
Group B

Abstract Introduction Antipsychotics are drugs that are widely prescribed for mental disorders, such as schizophrenia and psychosis. Recent in vitro studies show antipsychotics play a role in the initiation of neuronal cell apoptosis. This study aims to determine the effect of haloperidol and risperidone on neuronal cell apoptosis in Wistar white rats. Methods Male wistar rats aged 8 weeks (n = 30) were used in this study. Wistar rats were randomized into 6 groups. Group A: 5 wistar rats as a control without induced schizophrenia, aquades and drugs. Group B: 5 Wistar-induced psychotic mice (using 30 mg / kgBB ketamine, intraperitoneal injection for 5 days) and aquadest. Group C: 5 rats were induced psychotic and were given haloperidol or 0.05 mg / kgBB orally, for 28 days. Group D: 5 mice were induced psychotic and were given haloperidol 0.1 mg / kg orally, for 28 days. Group E: 5 mice were induced psychotic and were given risperidone 0.05 mg / kgBB orally, for 28 days. Group F: 5 mice were induced psychotic and given risperidone 0.1 mg / kgBB orally, for 28 days. Apoptosis of neuronal cells in the ventral tegmental area was assessed by caspase-3 immunohistochemistry. The colored area will be calculated as a total percentage using the imageJ program. Results Risperidone and haloperidol increase caspase-3 activity, but haloperidol increases caspase-3 activity more than risperidone. Conclussion Risperidone and haloperidol induce apoptosis of neuronal cells and tardive dyskinesia in Wistar rats with psychotic models.

Anticonvulsive and anti-epileptogenesis effects of Echinacea purpurea root extract, an involvement of CB2 receptor

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Masoumeh Gholami ◽  
Jamal Amri ◽  
Saeed Pazhoohan ◽  
Mehdi Sadegh
Keyword(s):  
Mortality Rate ◽  
Receptor Antagonist ◽  
Wistar Rats ◽  
Echinacea Purpurea ◽  
Root Extract ◽  
Cb2 Receptor ◽  
Kindling Model ◽  
Male Wistar Rats ◽  
Clonic Seizures ◽  
Cb2 Receptors

Abstract Objective Phytocannabinoids beyond the Δ9-tetrahy-drocannabinol have shown anticonvulsive effects. Also, alkylamides from Echinacea purpurea have been proved as cannabinomimetics. We examined the effect of the hydroalcoholic root extract of E. purpurea on pentylenetetrazol (PTZ)-induced tonic–clonic seizures and kindling model of epileptogenesis and the involvement of CB2 receptors as the mediator of this effect. Methods Male Wistar rats (200 ± 20 g) were used. Single intraperitoneal (i.p.) injection of PTZ (80 mg/kg) was used to induce tonic–clonic seizures. The kindling model of epileptogenesis was induced by daily injections of PTZ (37 mg/kg; i.p. for 15 days). Latency and duration of the stages were monitored for analysis. The hydroalcoholic root extract of E. purpurea was injected (i.p.) 20 min before seizure induction at the doses of 10, 50, 100 and 200 mg/kg. CB2 receptor antagonist SR144528 was injected (0.1 mg/kg; i.p.) 20 min before the Echinacea injection. Results In the tonic–clonic model, pretreatment with E. purpurea at the doses of 100 and 200 mg/kg significantly increased latencies to S2–S6, while it significantly decreased S6 duration and mortality rate. SR144528 injection before the injection of 100 mg/kg of E. purpurea significantly prevented the effects of the extract on S4–S6 latencies. In the kindling model, E. purpurea at the doses of 100 and 200 mg/kg significantly delayed epileptogenesis and decreased mortality rate, while SR144528 injection before the injection of 100 mg/kg of E. purpurea significantly blocked this effect of the extract. Conclusion These findings revealed the anticonvulsive and antiepileptogenesis effects of the E. purpurea root extract, which can be mediated by CB2 receptors.

5-HT2B-receptor antagonist LY-272015 is antihypertensive in DOCA-salt-hypertensive rats

1999 ◽  
Vol 276 (3) ◽  
pp. H944-H952 ◽  
Author(s):  
Stephanie W. Watts ◽  
Gregory D. Fink
Keyword(s):  
Blood Pressure ◽  
Receptor Antagonist ◽  
High Blood Pressure ◽  
Reduce Blood Pressure ◽  
Receptor Expression ◽  
Hypertensive Rats ◽  
Arterial Blood ◽  
Salt Hypertension

We previously demonstrated a change in the receptors mediating 5-hydroxytryptamine (5-HT)-induced contraction in arteries of deoxycorticosterone acetate (DOCA)-salt-hypertensive rats. Specifically, contraction to 5-HT is mediated primarily by 5-HT2A receptors in arteries from normotensive sham rats and by both 5-HT2A and 5-HT2B receptors in arteries from hypertensive rats. We hypothesized that the 5-HT2B receptor may play a role in maintaining the high blood pressure of DOCA-salt-hypertensive rats, and herein we provide data connecting in vitro and in vivo findings. The endothelium-denuded isolated superior mesenteric artery of DOCA-salt rats displayed a marked increase in maximum contraction to the newly available 5-HT2B-receptor agonist BW-723C86 compared with that of arteries from sham rats, confirming that the 5-HT2B receptor plays a greater role in 5-HT-induced contraction in arteries from DOCA-salt rats. In chronically instrumented rats, the 5-HT2B-receptor antagonist LY-272015 (0.3, 1.0, and 3.0 mg/kg iv at 30-min intervals) was given cumulatively 1 time/wk during 4 wk of continued DOCA-salt treatment. LY-272015 did not reduce blood pressure of the sham-treated rats at any time or dose. However, LY-272015 (1.0 and 3.0 mg/kg) significantly reduced mean blood pressure in a subgroup of week 3 (−20 mmHg) and week 4 DOCA-salt (−40 mmHg) rats that had extremely high blood pressure (mean arterial blood pressure ∼200 mmHg). Blockade of 5-HT2Breceptors by in vivo administration of LY-272015 (3.0 mg/kg) was verified by observing reduced 5-HT-induced contraction in rat stomach fundus, the tissue from which the 5-HT2B receptor was originally cloned. These data support the novel hypothesis that 5-HT2B-receptor expression is induced during the development of DOCA-salt hypertension and contributes to the maintenance of severe blood pressure elevations.

scholarly journals Enteral administration of soyabean lecithin enhanced lymphatic absorption of triacylglycerol in rats

2003 ◽  
Vol 90 (3) ◽  
pp. 565-571 ◽  
Author(s):  
Megumi Nishimukai ◽  
Hiroshi Hara ◽  
Yoritaka Aoyama
Keyword(s):  
Wistar Rats ◽  
Sodium Taurocholate ◽  
Lymph Flow ◽  
Lipid Absorption ◽  
Lymphatic Absorption ◽  
Mesenteric Lymph ◽  
Enteral Administration ◽  
Male Wistar Rats ◽  
Rat Bile

As the physiological roles of dietary lecithin have not yet been clearly defined, we examined the effects of lecithin on lipid absorption in male Wistar rats with a mesenteric lymph cannula. Lymphatic absorption was observed after the infusion of 1 ml emulsion containing 100 mg test oil emulsified with sodium taurocholate (10 g/l) in three separate experiments. Test oils (100 mg) were: soyabean oil (triacylglycerol (TG) source, SO) and soyabean oil + lecithin (75 mg soyabean oil+25 mg lecithin, LE) in Expt 1; SO, LE or soyabean oil + lysolecithin (75 mg soyabean oil plus 25 mg lysolecithin, LY) in Expt 2; hydrolysed soyabean oil (HSO) or HSO+lysolecithin (75 mg HSO+25 mg lysolecithin, HLY) in Expt 3. After LE and LY infusions, lymph flow and the lymphatic output of TG was higher than after SO infusion at 0-30 min and 0-90 min respectively (Expts 1 and 2). Lecithin-induced increases in lymph TG output remained constant when HSO was infused (Expt 3). There were no differences in the TG:phospholipid ratio in the lymph after infusion among the groups; nevertheless, the lymphatic output of TG was much higher after infusion with LE than with SO. Fatty acid was released more efficiently from SO than from LE and LY by in vitro digestion with rat bile–pancreatic juice. These present results demonstrate that a TG emulsion containing soyabean lecithin or its hydrolysates promote lymphatic TG output and suggest that the increases in TG absorption do not depend on TG digestion.

scholarly journals Direct Vasocontractile Activities of Bupivacaine Enantiomers on the Isolated Rat Thoracic Aorta

2010 ◽  
Vol 2010 ◽  
pp. 1-3 ◽  
Author(s):  
Mai Mukozawa ◽  
Ko Takakura ◽  
Maki Mizogami
Keyword(s):  
Thoracic Aorta ◽  
Wistar Rats ◽  
Krebs Solution ◽  
Male Wistar Rats ◽  
Rat Thoracic Aorta ◽  
Isolated Arteries ◽  
Isolated Rat

Background.In vitrostudies with isolated arteries have shown direct vasoactivity of racemic bupivacaine. However, there is little information on the direct vasoactivities of bupivacaine enantiomers, S(−)- and R(+)-bupivacaine.Methods. We performed functional examinations using isolated intact thoracic aortic rings from male Wistar rats. Changes in ring tension produced by S(−)-, R(+)-, or racemic bupivacaine were measured in Krebs solution.Results. S(−)-bupivacaine produced the strongest contraction of the three agents. R(+)-bupivacaine showed limited vasoconstriction. The effects of racemic bupivacaine were located between these two.Conclusion. Each bupivacaine enantiomer showed specific vasocontractile activity, which affects the activity of racemic bupivacaine.

Concomitant release of sialic acids and calcium by neuraminidase from rat aorta in situ

1988 ◽  
Vol 235 (1279) ◽  
pp. 139-144 ◽  
Keyword(s):  
Sialic Acid ◽  
Wistar Rats ◽  
Rat Aorta ◽  
Sialic Acids ◽  
Molar Ratio ◽  
Male Wistar Rats

Male Wistar rats were heparinized and killed with pentobarbital. The upper and lower ends of the aortae were cannulated and the blood was washed out with saline until the washings contained calcium and sialic-acid-reacting material at minimal concentrations. The aortae were perfused with neuraminidase for 15 min. This caused the appearance of calcium as well as of sialic acids in the perfusate in total amounts of about 5.3 nmol and about 3.6 nmol per aorta respectively. The molar ratio of about 1.5 is sufficiently close to that determined for the association of calcium with sialic acids in vitro to suggest that their association is similar in vivo .

Differential oxidative stress and DNA damage in rat brain regions and blood following chronic arsenic exposure

2008 ◽  
Vol 24 (4) ◽  
pp. 247-256 ◽  
Author(s):  
D Mishra ◽  
SJS Flora
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Drinking Water ◽  
Wistar Rats ◽  
Arsenic Exposure ◽  
Brain Regions ◽  
Single Strand ◽  
Male Wistar Rats ◽  
Chronic Arsenic Exposure ◽  
The Brain

Chronic arsenic poisoning caused by contaminated drinking water is a wide spread and worldwide problem particularly in India and Bangladesh. One of the possible mechanisms suggested for arsenic toxicity is the generation of reactive oxygen species (ROS). The present study was planned 1) to evaluate if chronic exposure to arsenic leads to oxidative stress in blood and brain – parts of male Wistar rats and 2) to evaluate which brain region of the exposed animals was more sensitive to oxidative injury. Male Wistar rats were exposed to arsenic (50 ppm sodium arsenite in drinking water) for 10 months. The brain was dissected into five major parts, pons medulla, corpus striatum, cortex, hippocampus, and cerebellum. A number of biochemical variables indicative of oxidative stress were studied in blood and different brain regions. Single-strand DNA damage using comet assay was also assessed in lymphocytes. We observed a significant increase in blood and brain ROS levels accompanied by the depletion of GSH/GSSG ratio and glucose-6-phosphate dehydrogenase (G6PD) activity in different brain regions of arsenic-exposed rats. Chronic arsenic exposure also caused significant single-strand DNA damage in lymphocytes as depicted by comet with a tail in arsenic-exposed cells compared with the control cells. On the basis of results, we concluded that the cortex region of the brain was more sensitive to oxidative injury compared with the other regions studied. The present study, thus, leads us to suggest that arsenic induces differential oxidative stress in brain regions with cortex followed by hippocampus and causes single-strand DNA damage in lymphocytes.

scholarly journals Fructose-Drinking Water Induced Nonalcoholic Fatty Liver Disease and Ultrastructural Alteration of Hepatocyte Mitochondria in Male Wistar Rat

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Norshalizah Mamikutty ◽  
Zar Chi Thent ◽  
Farihah Haji Suhaimi
Keyword(s):  
Metabolic Syndrome ◽  
Drinking Water ◽  
Liver Disease ◽  
Fatty Liver Disease ◽  
Wistar Rats ◽  
Wistar Rat ◽  
Ultrastructural Changes ◽  
Nonalcoholic Fatty Liver ◽  
The Metabolic Syndrome ◽  
Male Wistar Rats

Background.Nonalcoholic fatty liver disease (NAFLD) is one of the complications of the metabolic syndrome. It encompasses a wide range of disease spectrum from simple steatosis to liver cirrhosis. Structural alteration of hepatic mitochondria might be involved in the pathogenesis of NAFLD.Aims.In the present study, we used a newly established model of fructose-induced metabolic syndrome in male Wistar rats in order to investigate the ultrastructural changes in hepatic mitochondria that occur with fructose consumption and their association with NAFLD pathogenesis.Methods.The concentration of fructose-drinking water (FDW) used in this study was 20%. Six male Wistar rats were supplemented with FDW 20% for eight weeks. Body composition and metabolic parameters were measured before and after 8 weeks of FDW 20%. Histomorphology of the liver was evaluated and ultrastructural changes of mitochondria were assessed with transmission electron micrograph.Results.After 8 weeks of fructose consumption, the animals developed several features of the metabolic syndrome. Moreover, fructose consumption led to the development of macrovesicular hepatic steatosis and mitochondrial ultrastructural changes, such as increase in mitochondrial size, disruption of the cristae, and reduction of matrix density.Conclusion.We conclude that in male Wistar rat 8-week consumption of FDW 20% leads to NAFLD likely via mitochondrial structural alteration.

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