scholarly journals Effects of Clofibrate on Salt Loading-Induced Hypertension in Rats

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Antonio Cruz ◽  
Isabel Rodríguez-Gómez ◽  
Rocío Pérez-Abud ◽  
Miguel Ángel Vargas ◽  
Rosemary Wangensteen ◽  
...  

The effects of clofibrate on the hemodynamic and renal manifestations of increased saline intake were analyzed. Four groups of male Wistar rats were treated for five weeks: control, clofibrate (240 mg/kg/day), salt (2% via drinking water), andsalt+clofibrate. Body weight, systolic blood pressure (SBP), and heart rate (HR) were recorded weekly. Finally, SBP, HR, and morphologic, metabolic, plasma, and renal variables were measured. Salt increased SBP, HR, urinary isoprostanes, NOx, ET, vasopressin and proteinuria and reduced plasma freeT4(FT4) and tissueFT4andFT3versus control rats. Clofibrate prevented the increase in SBP produced by salt administration, reduced the sodium balance, and further reduced plasma and tissue thyroid hormone levels. However, clofibrate did not modify the relative cardiac mass, NOx, urinary ET, and vasopressin of saline-loaded rats. In conclusion, chronic clofibrate administration prevented the blood pressure elevation of salt-loaded rats by decreasing sodium balance and reducing thyroid hormone levels.

1981 ◽  
Vol 59 (8) ◽  
pp. 872-875 ◽  
Author(s):  
Murray C. Macdonald ◽  
Robert L. Kline ◽  
Gordon J. Mogenson

Male Wistar rats chronically fed a low level (0.41%) of linoleic acid (LA) in the diet as supplied by 5% olive oil developed a significant elevation of systolic blood pressure as compared with rats fed either a medium (4.2%) or high (9.4%) level of dietary LA. Chronic excess intake of NaCl (3.75% in the diet) was associated with a significant elevation of blood pressure on all three diets but a low level of LA in the diet exaggerated the salt-induced hypertension. The results suggest that inadequate dietary LA may result in an increase in systolic blood pressure regardless of the sodium content of the diet.


Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Erminia Donnarumma ◽  
Emma Mitidieri ◽  
Teresa Tramontano ◽  
Vincenzo Brancaleone ◽  
Mariarosaria Bucci ◽  
...  

Introduction: Glucocorticoid (GC) excess is related to hypertension. The deletion of endothelial GC-receptors abrogates the blood pressure increase, suggesting GC-induced hypertension is endothelium-dependent. In response to shear stress endothelium releases nitric oxide, endothelial derived hyperpolarizing factor (EDHF) and prostacyclin. Recently H2S has been proposed as a candidate for EDHF. H2S is mainly produced by the enzymes cystathionine β-synthase (CBS) and cystathionine γ-lyase (CSE) from L-cysteine. The aim of this study was to investigate the EDHF/H2S signaling in GC-hypertension. Methods: Male Wistar rats were treated with DEX (1.5 mg/kg/sc) or vehicle (VEH) for 8 days. Systolic blood pressure (SBP) was monitored every 2 days. EDHF was evaluated in mesenteric plexus and carotid artery performing a concentration-effect curve of acetylcholine in presence of indomethacin (INDO) and nitro-L-arginine methyl ester (L-NAME). Apamin (APA) plus charibdotoxin (CTX), SKCa and BKCa inhibitors, or propargylglycine (PAG), CSE inhibitor, were used. CBS and CSE levels were analyzed by immunoblot. H2S levels were measured by a colorimetric assay. Results: DEX treatment significantly increased SBP compared to VEH (*p<0.05, **p<0.01, ***p<0.001 at days 2-4, 6, 8 respectively). EDHF-mediated relaxation of mesenteric bed or carotid artery was markedly reduced in DEX group compared to VEH (***p<0.001). APA and CTX as well as PAG abolished EDHF-mediated relaxation in DEX or VEH group (***,°°°p<0.001 respectively). CBS and CSE levels were significantly reduced in mesenteric plexus and carotid artery in DEX group (*p<0.05). The H2S production was markedly reduced in mesenteric plexus and carotid artery (*p<0.05, **p<0.01 respectively) as well as plasmatic H2S levels (*p<0.05) in DEX rats compared to VEH. Conclusions: Our data demonstrate that GC-excess induces an impairment of H2S/EDHF signaling indicating an additional cause of GC-mediated hypertension.


1975 ◽  
Vol 48 (5) ◽  
pp. 457-460
Author(s):  
T. Saruta ◽  
R. Nakamura ◽  
I. Saito ◽  
K. Kondo ◽  
S. Matuki

1. A large dose of oestrogen elevated the blood pressure in male Wistar rats. 2. Plasma renin substrate and renin activity increased significantly but plasma renin concentration was unchanged. 3. The increase in blood pressure induced by oestrogen was significantly reduced by salt loading, plasma renin concentration was suppressed and the increase in plasma renin activity was reduced. 4. The increase in plasma renin activity induced by the increase of plasma renin substrate concentration may play a role in oestrogen-induced elevation of blood pressure.


2011 ◽  
Vol 26 (suppl 1) ◽  
pp. 57-59 ◽  
Author(s):  
Marcio Wilker Soares Campelo ◽  
Ana Paula Bomfim Soares Campelo ◽  
Luiz Gonzaga de França Lopes ◽  
Armenio Aguiar dos Santos ◽  
Sergio Botelho Guimarães ◽  
...  

PURPOSE: To evaluate the effect of Rut-bpy (Cis-[Ru(bpy)2(SO3)(NO)]PF 6), a novel nitric oxide donor in Nω-nitro-L-arginine methyl ester (L-NAME)-induced hypertensive rats. METHODS: Twenty-four male Wistar rats were randomly assigned to four groups (n=6), named according to the treatment applied (G1-Saline, G2-Rut-bpy, G3-L-NAME and G4-L-NAME+Rut-bpy). L-NAME (30 mg/Kg) was injected intraperitoneally 30 minutes before the administration of Rut-bpy (100 mg/Kg). Mean abdominal aorta arterial blood pressure (MAP) was continuously monitored. RESULTS: Mean arterial blood pressure (MAP) in G3 rats rose progressively, reaching 147±16 mmHg compared with 100±19 mm Hg in G1 rats (p<0.05). In G4 rats, treated with L-NAME+Rut-bpy, MAP reached 149+11 mm Hg while in G2 rats, treated with Rut-bpy, MAP values were 106±11 mm Hg. In G1 rats these values decreased progressively reaching 87+14 mm Hg after 30 minutes. An important finding was the maintenance of the MAP throughout the experiment in G2 rats. CONCLUSION: Rut-bpy does not decrease the MAP in L-Name induced hypertensive rats. However, when it is used in anesthetized hypotensive rats a stable blood pressure is obtained.


2019 ◽  
Vol 50 (4) ◽  
pp. 725-737 ◽  
Author(s):  
Sadia Berzou ◽  
Djamil Krouf ◽  
Nawal Taleb-Dida ◽  
Akila Guenzet

Purpose The purpose of this study is to evaluate the effects of flaxseed (L. usitatissimum [Linn]) on blood pressure, redox status markers and acetylcholinesterase enzyme activity in ouabain-induced hypertension in normal Wistar rats. Design/methodology/approach Male Wistar rats weighing 250 ± 7 g (n = 24) fed with an experimental diet containing 20 per cent casein were divided into three groups (n = 8) and received a daily subcutaneous injection of either 0.9 per cent saline solution (T group) or 10 µg/kg/day of ouabain diluted in saline solution-treated Oub-Lu or not with 1 per cent of flaxseed (L. usitatissimum) mixed in the diet for 21 days. Findings The results showed that treatment with flaxseed had a significant effect (p < 0.05) in decreasing systolic, diastolic blood pressure, mean arterial pressure and the heart rate in hypertensive rats. Total and non-HDL cholesterol levels were reduced by –26 and –35 per cent; p = 0.04, respectively. Concentrations of thiobarbituric acid-reactive substances were significantly decreased by –85 and –42 per cent (p = 0.001 and p = 0.04), respectively in the plasma and heart. Nitric oxide levels were increased in the aorta (+ 63 per cent; p = 0.001). Moreover, in the heart and aorta, a significant increase was noted in the thiol contents (+81 and +69 per cent; p = 0.001, respectively), glutathione peroxidase (+50 per cent; p = 0.03 and p = 0.01, respectively) and acetylcholinesterase activities (75 and +19 per cent, respectively; p = 0.001 and p = 0.04). Originality/value These results suggest hypotensive, cardiomoderating and antioxidant effects of flaxseed in ouabain-induced hypertension in the rat. In addition, it promotes a significant increase of the acetylcholinesterase activity in tissues.


1990 ◽  
Vol 258 (4) ◽  
pp. R1042-R1050 ◽  
Author(s):  
R. A. Hebden ◽  
M. E. Todd ◽  
C. Tang ◽  
B. Gowen ◽  
J. H. McNeill

We investigated the effect of deoxycorticosterone acetate (DOCA)-induced hypertension on plasma lipid and cholesterol levels and the development of vascular atherosclerotic changes in male Wistar rats injected with streptozotocin (STZ) or saline (CON). Rats given STZ alone demonstrated a mild hyperlipidemia and hypercholesterolemia without any change in blood pressure. One week of DOCA administration was without effect on blood pressure in CON and STZ groups, but at 3 and 6 wk caused a significant and similar elevation in both groups. This DOCA-induced elevation in blood pressure appeared to be associated with the increase in plasma lipid and cholesterol levels seen in both CON and STZ groups at 3 and 6 wk, although the elevation in lipid and cholesterol levels was significantly more pronounced in the STZ rats. Both CON and STZ groups injected with DOCA developed significant pathological changes in all vessels under investigation. However, the degree of atherosclerosis appeared, from a semiquantitative analysis, to be worse in the thoracic aortas and renal arteries of the STZ group. Neither normotensive group developed any atherosclerosis. It is concluded that hypertension is associated with atherosclerosis in normal rats and rats with short-term STZ-induced diabetes mellitus, although the higher plasma lipid and cholesterol levels of the latter group may potentiate the degree of vascular damage.


2018 ◽  
Vol 10 (1) ◽  
pp. 76-85
Author(s):  
Elena Olivares-Álvaro ◽  
María Belén Ruiz-Roso ◽  
Mercedes Klett-Mingo ◽  
Sandra Ballesteros ◽  
Ricardo Gredilla ◽  
...  

Background:Aldosterone plays a key role in the development of endothelial dysfunction and hypertension. The regulation of biogenesis and fusion/fission processes of vascular mitochondria has not been examined in aldosterone-induced hypertension. Thereby, we sought to explore in greater depth the role of aldosterone in mitochondrial biogenesis and fusion/fission processes in hypertension and the associated increases in oxidative stress.Methods:Male Wistar rats received aldosterone (1mg/Kg/day) + 1% NaCl as drinking water for 3 weeks.Results:Systolic blood pressure was elevated (p<0.05) in aldosterone-treated rats. eNOS and p-eNOSSer1177protein expression was down regulated (p<0.05) and NADPH oxidase subunit p22phox expression was increased (p<0.05) in aldosterone-treated rats. Expression of mitochondrial biogenesis proteins SIRT1, PGC1α, PPARγ, and TFAM decreased (p<0.05) in aldosterone-treated rats. Protein expression of vascular DRP1, OMA1 and S-OPA1 up regulated (p<0.05) in aldosterone-treated rats. MFN1 and L-OPA1 (p<0.05) decreased in aldosterone-treated animals.Conclusion:The results showed that, in aldosterone-treated rats, hypertension is likely associated with increased oxidative stress in the aorta and with changes in the regulation of two key mitochondrial processes such as biogenesis and fusion/fission processes. The overall mitochondrial alterations observed in the study may play a role in aldosterone-derived vascular oxidative stress and hypertension.


Sign in / Sign up

Export Citation Format

Share Document