scholarly journals NIFEDIPINEON;

2019 ◽  
Vol 26 (02) ◽  
Author(s):  
Sidra Hamid ◽  
Qaiser Aziz ◽  
Aneela Jamil ◽  
Lubna Meraj ◽  
Shazia Muazam ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Luteinizing Hormone ◽  
Serum Testosterone ◽  
Serum Testosterone Level ◽  
Control Group ◽  
Channel Blockers ◽  
Sprague Dawley ◽  
Study Objective ◽  
Serum Luteinizing Hormone ◽  
Sprague Dawley Rats

Background: The most potent and effective drugs used for the management of blood pressure in hypertensive patients are Calcium channel blockers (CCBs). Nifedipine, a CCB, acts by blocking entry of calcium ions all the way through the voltage gated calcium channels (VGCCs) of L-type present in the smooth muscle cells of blood vesselsand reducing the blood pressure by decreasing the peripheral vascular resistance. Objectives: The study objective was to determine the effect of nifedipine on serum luteinizing hormone (LH) and serum testosterone in male Sprague Dawley rats. Study Design: Animal experimental study. Setting: All experiments were conducted at the Research laboratory of Shifa College of Medicine, Islamabad along with National Institute of Health (NIH), Islamabad. Period: October, 2012 to April, 2014. Methods: The study was done on adult male Sprague-Dawley rats (N= 60) aged 90-120 days old and their body weights varied between 200 + 50 grams. Rats were divided intotwo groups (n=30). Group A was administered0.5 ml distilled water/rat daily orally, group B was administered orally with nifedipine 50 mg/kg/rat dissolved in 1ml of DMSO. All the doses were given to rats for 8 weeks. After 8 weeks, serum luteinizing hormone and serum testosterone were measured in both groups. Results: In Nifedipine treated group, serum testosterone was significantly decreasedand serum LH was unaffected as compared to the control group. Conclusion: Nifedipine has adverse effects on male fertility as it decreases serum testosterone level.

Effect of Cordyceps Militaris Supplementation on Sperm Production, Sperm Motility and Hormones in Sprague-Dawley Rats

2008 ◽  
Vol 36 (05) ◽  
pp. 849-859 ◽  
Author(s):  
Ying Chang ◽  
Kee-Ching Jeng ◽  
Kuei-Fen Huang ◽  
Ying-Chung Lee ◽  
Chien-Wei Hou ◽  
...  
Keyword(s):  
Direct Evidence ◽  
Treatment Time ◽  
Sperm Quality ◽  
Sperm Count ◽  
Serum Testosterone ◽  
Cordyceps Militaris ◽  
Control Group ◽  
Epididymal Sperm ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

Cordyceps species have been traditionally used as for the enhancement of sexual function, but its direct evidence is lacking. We investigated the spermatogenic effect of Cordyceps militaris (CM) as supplementation with CM mycelium to 7-week-old male Sprague-Dawley (SD) rats. Ninety rats (30 for each group) were selected to regular diet or diet supplemented with CM mycelium (1% and 5%) for 6 weeks. Epididymal sperm were collected from 6 animals per group at each interval of observation. They were allowed to recover for one week. The quality and quantity of sperm were compared in these rats. The CM supplementation resulted in an increase of serum cordycepin concentration ( n = 6, each group) that correlated with treatment time and the cordycepin level was significantly higher ( p < 0.05) in 5% group as compared to 1% group at the 5th and 6th week. Epididymal sperm count was enhanced significantly from the control, at the 5th week and peaked at the 6th week in both groups supplemented with CM (each time point, n = 6; p < 0.05) and maintained for 2 weeks after stopping the treatment. Increased serum testosterone and estradiol-17 (E2) concentrations were found in rats with the CM supplementation ( p < 0.05), but not other hormones such as follicle stimulating hormone (FSH), luteinizing hormone (LH) or prolactin. Importantly, percentages of motile sperm cells were also enhanced significantly ( p < 0.05) paralleled the serum testosterone pattern from the supplement groups as compared to the control group. Taken together, these results indicate that supplementation with CM improves sperm quality and quantity in rats.

scholarly journals Food emulsifier glycerin monostearate aggravates phthalates’ testicular toxicity by disrupting tight junctions’ barrier function in rats

2021 ◽  
Author(s):  
Ling-Zi Xia ◽  
Min Yang ◽  
Miao He ◽  
Ming-Zhe Jiang ◽  
Chang Qin ◽  
...  
Keyword(s):  
Tight Junctions ◽  
Serum Testosterone ◽  
The Body ◽  
Serum Testosterone Level ◽  
Control Group ◽  
Ultrastructural Observation ◽  
Testis Weight ◽  
Testicular Toxicity ◽  
Sprague Dawley ◽  
Food Emulsifier

Abstract Objectives This study was aimed to investigate the effect of widely used food emulsifier glycerin monostearate (GM) on testicular toxicity caused by the mixture of three commonly used PEs (MPEs) in rats, and further to explore the underlying mechanism. Materials and Methods Thirty male Sprague-Dawley rats were divided into three groups randomly. Rats were orally treated with 160 mg/kg/d MPEs in MPEs group; Rats were coinstantaneously treated with 160 mg/kg/d MPEs and 200 mg/kg/d GM in MPEs+GM group; Rats were treated with the excipient in control group. The intervention last for 5 weeks. Testis weight, epididymis weight, testicular histopathology and serum testosterone were detected for testicular toxicity evaluation. The testicular ultrastructure, the tight junction proteins zonula occluden (ZO)-1 and claudin were measured for the mechanism exploration. Results The body weight, epididymis, serum testosterone level, and anogenital distance in MPEs+GM group were significantly decreased comparing with control group (P&lt;0.05); Testicular histopathological observation showed that shed spermatids were observed in MPEs+GM group. Ultrastructural observation of testicular cells showed that the cristae number was decreased in some mitochondrion in MPEs group, whereas the cristae was fused and disappeared in most mitochondrion in MPEs+GM group. The tight junctions were broken in MPEs+GM group, meanwhile, the expression of ZO-1 and claudin were altered in MPEs+GM group (P&lt;0.01). Conclusions The results from this study indicated that GM aggravated MPEs’ testicular toxicity, which might relate to the injured mitochondrion and damaged tight junctions in testicular tissue.

Sodium—Potassium Pump Activity in Mineralocorticoid- and Glucocorticoid-Induced Hypertension

1982 ◽  
Vol 63 (s8) ◽  
pp. 69s-72s ◽  
Author(s):  
G. Wambach ◽  
A. Helber ◽  
W. Kaufmann
Keyword(s):  
Blood Pressure ◽  
Atpase Activity ◽  
Systolic Blood Pressure ◽  
Heart Tissue ◽  
Control Group ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Induced Hypertension ◽  
Pump Activity ◽  
Kidney Liver

1. The activity of ouabain-sensitive Na+,K+-dependent ATPase and ouabain-sensitive ATPase was measured in the microsomal fractions of kidney, liver and heart tissue of Sprague-Dawley rats treated with DOCA (10 mg day−1 kg−1 for 6 days, systolic blood pressure 143 ± 13 mmHg, n = 9) or 6 α-methylprednisolone (100 mg day−1 kg−1 for 6 days, systolic blood pressure 140 ± 19 mmHg, n = 9) and of a control group (systolic blood pressure 124 ± 12 mmHg, n = 9). 2. In the kidney, the ouabain-sensitive Na+,K+-ATPase activity (μmol of phosphate h−1 mg−1 of protein) was increased in the DOCA-treated (33.0 ± 6.9) and in the prednisolone-treated groups (30.8 ± 6.9) compared with that in the control group (26.4 ± 3.4) (P < 0.05). In the liver, the ouabain-sensitive Na+,K+-ATPase activity was elevated in the prednisolone-treated animals only (4.8 ± 1.3 vs 3.1 ± 0.8 in the controls, P < 0.025). The ouabain-sensitive Na+,K+-ATPase activity in heart tissue was similar in all three groups. The ouabain-insensitive ATPase activity was not altered by DOCA or prednisolone in the tissues studied. 3. In a separate study, the activity of the ouabain-sensitive Na+,K+-ATPase in erythrocyte ghosts was found to be elevated in 10 patients with Cushing's syndrome (0.91 ± 0.35 μmol of phosphate h−1 mg−1 of protein) compared with five patients with primary aldosteronism and compared with 12 normotensive control subjects (0.38 ± 0.08) (P < 0.005). 4. These data demonstrate an increased Na-K pump activity in the kidney in mineralocorticoid-induced hypertension. Glucocorticoids in addition activate the Na-K pump in a variety of other tissues. This could partially explain the redistribution of volume from the intracellular to the extracellular space.

scholarly journals Increased superoxide levels in ganglia and sympathoexcitation are involved in sarafotoxin 6c-induced hypertension

2008 ◽  
Vol 295 (5) ◽  
pp. R1546-R1554 ◽  
Author(s):  
Melissa Li ◽  
Xiaoling Dai ◽  
Stephanie Watts ◽  
David Kreulen ◽  
Gregory Fink
Keyword(s):  
Blood Pressure ◽  
Sympathetic Innervation ◽  
Sympathetic Ganglia ◽  
Plasma Norepinephrine ◽  
Sprague Dawley ◽  
Surgical Ablation ◽  
Arterial Blood ◽  
Sprague Dawley Rats ◽  
Induced Hypertension ◽  
Hypertension Development

Endothelin (ET) type B receptors (ETBR) are expressed in multiple tissues and perform different functions depending on their location. ETBR mediate endothelium-dependent vasodilation, clearance of circulating ET, and diuretic effects; all of these should produce a fall in arterial blood pressure. However, we recently showed that chronic activation of ETBR in rats with the selective agonist sarafotoxin 6c (S6c) causes sustained hypertension. We have proposed that one mechanism of this effect is constriction of capacitance vessels. The current study was performed to determine whether S6c hypertension is caused by increased generation of reactive oxygen species (ROS) and/or activation of the sympathetic nervous system. The model used was continuous 5-day infusion of S6c into male Sprague-Dawley rats. No changes in superoxide anion levels in arteries and veins were found in hypertensive S6c-treated rats. However, superoxide levels were increased in sympathetic ganglia from S6c-treated rats. In addition, superoxide levels in ganglia increased progressively the longer the animals received S6c. Treatment with the antioxidant tempol impaired S6c-induced hypertension and decreased superoxide levels in ganglia. Acute ganglion blockade lowered blood pressure more in S6c-treated rats than in vehicle-treated rats. Although plasma norepinephrine levels were not increased in S6c hypertension, surgical ablation of the celiac ganglion plexus, which provides most of the sympathetic innervation to the splanchnic organs, significantly attenuated hypertension development. The results suggest that S6c-induced hypertension is partially mediated by sympathoexcitation to the splanchnic organs driven by increased oxidative stress in prevertebral sympathetic ganglia.

scholarly journals Skeletal Muscle Metabolomic Responses to Endurance and Resistance Training in Rats under Chronic Unpredictable Mild Stress

2021 ◽  
Vol 18 (4) ◽  
pp. 1645
Author(s):  
Xiangyu Liu ◽  
Xiong Xue ◽  
Junsheng Tian ◽  
Xuemei Qin ◽  
Shi Zhou ◽  
...  
Keyword(s):  
Resistance Exercise ◽  
Endurance Exercise ◽  
Field Tests ◽  
Treadmill Running ◽  
Control Group ◽  
Mild Stress ◽  
Chronic Unpredictable Mild Stress ◽  
Sprague Dawley ◽  
Exercise Interventions ◽  
Sprague Dawley Rats

The objectives of this study were to compare the antidepressant effects between endurance and resistance exercise for optimizing interventions and examine the metabolomic changes in different types of skeletal muscles in response to the exercise, using a rat model of chronic unpredictable mild stress (CUMS)-induced depression. There were 32 male Sprague-Dawley rats randomly divided into a control group (C) and 3 experimental groups: CUMS control (D), endurance exercise (E), and resistance exercise (R). Group E underwent 30 min treadmill running, and group R performed 8 rounds of ladder climbing, 5 sessions per week for 4 weeks. Body weight, sucrose preference, and open field tests were performed pre and post the intervention period for changes in depressant symptoms, and the gastrocnemius and soleus muscles were sampled after the intervention for metabolomic analysis using the 1H-NMR technique. The results showed that both types of exercise effectively improved the depression-like symptoms, and the endurance exercise appeared to have a better effect. The levels of 10 metabolites from the gastrocnemius and 13 metabolites from the soleus of group D were found to be significantly different from that of group C, and both types of exercise had a callback effect on these metabolites, indicating that a number of metabolic pathways were involved in the depression and responded to the exercise interventions.

Ranitidine as an alcohol dehydrogenase inhibitor in acute methanol toxicity in rats

2009 ◽  
Vol 29 (2) ◽  
pp. 93-101 ◽  
Author(s):  
Amal A El-Bakary ◽  
Sahar A El-Dakrory ◽  
Sohayla M Attalla ◽  
Nawal A Hasanein ◽  
Hala A Malek
Keyword(s):  
Alcohol Dehydrogenase ◽  
High Performance ◽  
Negative Control Group ◽  
Positive Control ◽  
Negative Control ◽  
Control Group ◽  
Sprague Dawley ◽  
Blood Samples ◽  
Methanol Poisoning ◽  
Sprague Dawley Rats

Methanol poisoning is a hazardous intoxication characterized by visual impairment and formic acidemia. The therapy for methanol poisoning is alcohol dehydrogenase (ADH) inhibitors to prevent formate accumulation. Ranitidine has been considered to be an inhibitor of both gastric alcohol and hepatic aldehyde dehydrogenase enzymes. This study aimed at testing ranitidine as an antidote for methanol acute toxicity and comparing it with ethanol and 4-methyl pyrazole (4-MP). This study was conducted on 48 Sprague-Dawley rats, divided into 6 groups, with 8 rats in each group (one negative control group [C1], two positive control groups [C2, C3] and three test groups [1, 2 and 3]). C2, C3 and all test groups were exposed to nitrous oxide by inhalation, then, C3 group was given methanol (3 g/kg orally). The three test groups 1, 2 and 3 were given ethanol (0.5 g/kg orally), 4-MP (15 mg/kg intraperitoneally) and ranitidine (30 mg/kg intraperitoneally), respectively, 4 hours after giving methanol. Rats were sacrificed and heparinized, cardiac blood samples were collected for blood pH and bicarbonate. Non-heparinized blood samples were collected for formate levels by high performance liquid chromatography. Eye balls were enucleated for histological examination of the retina. Ranitidine corrected metabolic acidosis (p = .025), decreased formate levels (p = .014) and improved the histological findings in the retina induced by acute methanol toxicity.

Proximal tubule microvilli remodeling and albuminuria in the Ren2 transgenic rat

2007 ◽  
Vol 292 (2) ◽  
pp. F861-F867 ◽  
Author(s):  
Melvin R. Hayden ◽  
Nazif A. Chowdhury ◽  
Shawna A. Cooper ◽  
Adam Whaley-Connell ◽  
Javad Habibi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Proximal Tubule ◽  
Structural Damage ◽  
Kidney Tissue ◽  
Proximal Tubule Cell ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

TG(mRen2)27 (Ren2) transgenic rats overexpress the mouse renin gene, with subsequent elevated tissue ANG II, hypertension, and nephropathy. The proximal tubule cell (PTC) is responsible for the reabsorption of 5–8 g of glomerular filtered albumin each day. Excess filtered albumin may contribute to PTC damage and tubulointerstitial disease. This investigation examined the role of ANG II-induced oxidative stress in PTC structural remodeling: whether such changes could be modified with in vivo treatment with ANG type 1 receptor (AT1R) blockade (valsartan) or SOD/catalase mimetic (tempol). Male Ren2 (6–7 wk old) and age-matched Sprague-Dawley rats were treated with valsartan (30 mg/kg), tempol (1 mmol/l), or placebo for 3 wk. Systolic blood pressure, albuminuria, N-acetyl-β-d-glucosaminidase, and kidney tissue malondialdehyde (MDA) were measured, and ×60,000 transmission electron microscopy images were used to assess PTC microvilli structure. There were significant differences in systolic blood pressure, albuminuria, lipid peroxidation (MDA and nitrotyrosine staining), and PTC structure in Ren2 vs. Sprague-Dawley rats (each P < 0.05). Increased mean diameter of PTC microvilli in the placebo-treated Ren2 rats ( P < 0.05) correlated strongly with albuminuria ( r2 = 0.83) and moderately with MDA ( r2 = 0.49), and there was an increase in the ratio of abnormal forms of microvilli in placebo-treated Ren2 rats compared with Sprague-Dawley control rats ( P < 0.05). AT1R blockade, but not tempol treatment, abrogated albuminuria and N-acetyl-β-d-glucosaminidase; both therapies corrected abnormalities in oxidative stress and PTC microvilli remodeling. These data indicate that PTC structural damage in the Ren2 rat is related to the oxidative stress response to ANG II and/or albuminuria.

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