Hemodynamic and Metabolic Effects of Hypomagnesemia in Spontaneously Hypertensive Rats

Cardiology ◽  
1988 ◽  
Vol 75 (2) ◽  
pp. 81-89 ◽  
Author(s):  
Steven G. Chrysant ◽  
Louis Ganousis ◽  
Catherine Chrysant
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Metabolic Effects ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Metabolic effects of telmisartan in spontaneously hypertensive rats

2006 ◽  
Vol 373 (4) ◽  
pp. 264-270 ◽  
Author(s):  
Yong-Qi Li ◽  
Hui Ji ◽  
Yi-Hua Zhang ◽  
Da-Yong Ding ◽  
Xiao-Lei Ye
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Metabolic Effects ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Lack of beneficial metabolic effects of quercetin in adult spontaneously hypertensive rats

2010 ◽  
Vol 627 (1-3) ◽  
pp. 242-250 ◽  
Author(s):  
Miguel Romero ◽  
Rosario Jiménez ◽  
Belén Hurtado ◽  
Juan Manuel Moreno ◽  
Isabel Rodríguez-Gómez ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Metabolic Effects ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Pineal Hyperactivity in Spontaneously Hypertensive Rats: Muscarinic Regulation of Indole Metabolism

1990 ◽  
Vol 79 (5) ◽  
pp. 437-442 ◽  
Author(s):  
Liliana M. E. Finocchiaro ◽  
Angelika Scheucher ◽  
Azucena L. Alvarez ◽  
Samuel Finkielman ◽  
Victor E. Nahmod ◽  
...  
Keyword(s):  
Pineal Gland ◽  
Binding Sites ◽  
Spontaneously Hypertensive Rats ◽  
Electrical Field Stimulation ◽  
Metabolic Effects ◽  
Hypertensive Rats ◽  
Electrical Field ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Wistar Kyoto

1. Choline acetyltransferase activity and [3H]quinuclidinyl benzylate-binding sites were detected in the pineal gland of normotensive Wistar—Kyoto rats and of spontaneously hypertensive rats. 2. In vitro, muscarinic activation by pilocarpine increased the pineal metabolic production of hydroxyindole derivatives up to 5-hydroxytryptamine and produced a less marked stimulation of melatonin biosynthesis. 3. Electrical field stimulation of pineal gland slices caused similar metabolic effects. 4. Muscarinic blockade with atropine inhibited the effects on hydroxyindole metabolism. 5. [3H]Quinuclidinyl benzylate-binding sites, indicative of muscarinic receptors, were more numerous, and basal 5-hydroxytryptamine and melatonin levels were higher, in the pineal gland of spontaneously hypertensive rats compared with Wistar—Kyoto rats. 6. The atropine-sensitive metabolic effects of pilocarpine and electrical field stimulation on the pineal gland were increased in spontaneously hypertensive rats compared with Wistar-Kyoto rats.

scholarly journals Hepatotoxic Effects of Fenofibrate in Spontaneously Hypertensive Rats Expressing Human C-Reactive Protein

2016 ◽  
pp. 891-899 ◽  
Author(s):  
V. ŠKOP ◽  
J. TRNOVSKÁ ◽  
O. OLIYARNYK ◽  
I. MARKOVÁ ◽  
H. MALÍNSKÁ ◽  
...  
Keyword(s):  
Body Weight ◽  
Spontaneously Hypertensive Rats ◽  
Hdl Cholesterol ◽  
Metabolic Effects ◽  
C Reactive Protein ◽  
Hypertensive Rats ◽  
Serum Triglycerides ◽  
Spontaneously Hypertensive ◽  
Reactive Protein ◽  
Anti Inflammatory

Dyslipidemia and inflammation play an important role in the pathogenesis of cardiovascular and liver disease. Fenofibrate has a well-known efficacy to reduce cholesterol and triglycerides. Combination with statins can ameliorate hypolipidemic and anti-inflammatory effects of fibrates. In the current study, we tested the anti-inflammatory and metabolic effects of fenofibrate alone and in combination with rosuvastatin in a model of inflammation and metabolic syndrome, using spontaneously hypertensive rats expressing the human C-reactive protein transgene (SHR-CRP transgenic rats). SHR-CRP rats treated with fenofibrate alone (100 mg/kg body weight) or in combination with rosuvastatin (20 mg/kg body weight) vs. SHR-CRP untreated controls showed increased levels of proinflammatory marker IL6, increased concentrations of ALT, AST and ALP, increased oxidative stress in the liver and necrotic changes of the liver. In addition, SHR-CRP rats treated with fenofibrate, or with fenofibrate combined with rosuvastatin vs. untreated controls, exhibited increased serum triglycerides and reduced HDL cholesterol, as well as reduced hepatic triglyceride, cholesterol and glycogen concentrations. These findings suggest that in the presence of high levels of human CRP, fenofibrate can induce liver damage even in combination with rosuvastatin. Accordingly, these results caution against the possible hepatotoxic effects of fenofibrate in patients with high levels of CRP.

scholarly journals Age-related autocrine diabetogenic effects of transgenic resistin in spontaneously hypertensive rats: gene expression profile analysis

2011 ◽  
Vol 43 (7) ◽  
pp. 372-379 ◽  
Author(s):  
Michal Pravenec ◽  
Václav Zídek ◽  
Vladimír Landa ◽  
Miroslava Šimáková ◽  
Petr Mlejnek ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Adipose Tissue ◽  
Glucose Intolerance ◽  
Spontaneously Hypertensive Rats ◽  
Metabolic Effects ◽  
Related Factor ◽  
Hypertensive Rats ◽  
Transgenic Rats ◽  
Spontaneously Hypertensive

Increased circulating levels of resistin have been proposed as a possible link between obesity and insulin resistance; however, many of the potential metabolic effects of resistin remain to be investigated, including systemic versus local resistin action. We investigated potential autocrine effects of resistin on lipid and glucose metabolism in 2- and 16-mo-old transgenic spontaneously hypertensive rats (SHR) expressing a nonsecreted form of mouse resistin under control of the aP2 promoter. To search for possible molecular mechanisms, we compared gene expression profiles in adipose tissue in 6-wk-old transgenic SHR versus control rats, before development of insulin resistance, by digital transcriptional profiling using high-throughput sequencing. Both young and old transgenic rats showed moderate expression of the resistin transgene in adipose tissue but had serum resistin levels similar to control SHR and undetectable levels of transgenic resistin in the circulation. Young transgenic rats exhibited mild glucose intolerance. In contrast, older transgenic rats displayed marked glucose intolerance in association with near total resistance of adipose tissue to insulin-stimulated glucose incorporation into lipids (6 ± 2 vs. 77 ± 19 nmol glucose·g−1·2 h−1, P < 0.00001). Ingenuity Pathway Analysis of differentially expressed genes revealed calcium signaling, Nuclear factor-erythroid 2-related factor-2 (NRF2)-mediated oxidative stress response, and actin cytoskeletal signaling canonical pathways as those most significantly affected. Analysis using DAVID software revealed oxidative phosphorylation, glutathione metabolism, pyruvate metabolism, and peroxisome proliferator-activated receptor (PPAR) signaling as top Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. These results suggest that with increasing age autocrine effects of resistin in fat tissue may predispose to diabetes in part by impairing insulin action in adipose tissue.

scholarly journals Acute Toxic Effects of Telmisartan in Spontaneously Hypertensive Rats Fed a High Fructose Diet

2018 ◽  
pp. 851-856
Author(s):  
J. ŠILHAVÝ ◽  
P. MLEJNEK ◽  
M. ŠIMÁKOVÁ ◽  
I. VANĚČKOVÁ ◽  
M. BEHULIAK ◽  
...  
Keyword(s):  
Body Weight ◽  
Spontaneously Hypertensive Rats ◽  
Toxic Effects ◽  
Metabolic Effects ◽  
Brown Norway ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
High Fructose Diet ◽  
High Fructose ◽  
Acute Toxic

Telmisartan is an angiotensin receptor blocker (ARB) and a selective peroxisome proliferator activated receptor gamma (PPARG) modulator. Recently, we tested metabolic effects of telmisartan (5 mg/kg body weight) in spontaneously hypertensive rats (SHR) fed a diet containing 60 % fructose, a widely used model of the metabolic syndrome. Surprisingly, we observed acute toxic effects of telmisartan. Rats lost body weight rapidly and died within 2 to 3 weeks due to bleeding into the upper gastrointestinal tract. SHR fed a high fructose diet and treated with telmisartan exhibited rapid decrease in blood pressure when compared to the SHR fed a high fructose diet and treated with valsartan. Concentrations of both unconjugated telmisartan and telmisartan glucuronide in the liver of SHR rats fed a high fructose diet were approximately 4 fold higher when compared to Brown Norway (BN) rats fed the same diet. Plasma concentrations of unconjugated telmisartan in the SHR were about 5 fold higher when compared to BN rats while plasma levels of telmisartan glucuronide were similar between the strains. Testing of other rat strains, diets, and the ARB valsartan showed that toxic effects of telmisartan in combination with high fructose diet are specific for the SHR. These results are consistent with the possibility that in some circumstances, SHR are predisposed to telmisartan toxicity possibly because of a genetically determined disturbance in telmisartan metabolism.

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