scholarly journals Long-Term Effect of an AqueousFraxinus excelsiorL. Seed Extract in Spontaneously Hypertensive Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Noemi López-Carreras ◽  
Sandra Fernández-Vallinas ◽  
Marta Miguel ◽  
Amaya Aleixandre

The effect of long-term intake of different doses (20, 40, and 60 mg/kg/day) of aFraxinus excelsiorL. seed extract (FESE) on spontaneously hypertensive rats (SHR) was evaluated. Water was used as control and captopril (50 mg/kg/day) was used as positive control. Systolic blood pressure, body weight, and food and liquid intake were registered weekly in SHR. The antioxidant and vascular relaxing properties of FESE were also studied in these animals. The development of hypertension was attenuated in the groups treated with captopril or FESE. The antihypertensive effect was more accentuated in the captopril group than in the FESE groups, and it was paradoxically more accentuated in the groups treated with 20 mg/kg/day or 40 mg/kg/day of FESE than in the group treated with the highest dose of this extract. Body weight gain and food intake increased in the FESE groups. After removing the corresponding antihypertensive treatment, the arterial blood pressure and the body weight of the FESE treated animals returned to control values. In addition, FESE increased plasma antioxidant capacity and decreased plasma and liver malondialdehyde levels. Moreover, acetylcholine relaxation improved in the aorta rings from the FESE treated rats.

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 699-700
Author(s):  
Christine Elise Barandier ◽  
Zhihong Yang ◽  
Thomas Felix Luscher

P38 It has been reported that some ET-receptor blockers prevent cerebral injury in stroke-prone spontaneously hypertensive rats (SPSHR), whereas chronic inhibition of nitric oxide synthase (NOS) precipitates stroke. We investigated the protective effects of chronic treatment with BSF208075, a selective ETA-receptor blocker in SPSHR treated with the NOS inhibitor, L-NAME, or untreated. 4 groups of male SPSHR, 10 week old, were studied: a control group and 3 groups treated with BSF208075 (30 mg/kg/day), L-NAME (10 mg/kg/day) or BSF208075+L-NAME (30 and 10 mg/kg/day, respectively). Systolic blood pressure, body weight and survival were recorded. In the control group, severe hypertension (292.3±1.0mmHg; p<0.01 vs baseline) developed within 4 weeks. In contrast, in the BSF208075-treated group, the development of hypertension (265.2±3.8mmHg; p<0.01 vs control) was limited and blood pressure started to decrease after 4 weeks of treatment. In both of these groups, the increase in body weight was normal and similar, and 90% of the animals were still alive after 50 days of treatment. In the L-NAME-treated group, the blood pressure immediately and drastically increased, the body weight was reduced by 50% within 6 weeks of treatment. 50% of mortality was observed after 22 days of treatment, and all rats died within 36 days. The mean survival was 25.9±2.4 days. In L-NAME+BSF208075-treated group, BSF208075, although it did not prevent the development of hypertension, it reduced the loss of body weight and increased mean survival to 36.7±1.4 days (p<0.01 vs L-NAME-treated group). In this group, 50% of mortality was observed after 37 days of treatment, and all rats died within 41 days. These results show that BSF208075 delays the development of hypertension in SPSHR, and increases survival of L-NAME-treated SPSHR, independent of hypertension.


1985 ◽  
Vol 69 (5) ◽  
pp. 511-515 ◽  
Author(s):  
P. J. O. Manhem ◽  
S. A. Clark ◽  
W. B. Brown ◽  
G. D. Murray ◽  
J. I. S. Robertson

1. Chlorothiazide (100 mg/kg body weight) was given by gavage daily to spontaneously hypertensive rats for 4 weeks. Another group of spontaneously hypertensive rats was given only tap water and served as control. 2. Measurements of total exchangeable sodium, blood pressure and weight were performed for 2 weeks before and for 4 weeks during treatment. 3. Before treatment, exchangeable sodium, blood pressure and weight were similar in the two groups of rats. 4. Chlorothiazide significantly attenuated the blood pressure increase in spontaneously hypertensive rats, the effect being most marked during the first 2 1/2 weeks of treatment and less thereafter. 5. Rats in the chlorothiazide-treated group gained weight more slowly than did those of the control group. 6. Exchangeable sodium, expressed as mmol/kg body weight, did not differ significantly between the two groups at any stage. 7. When exchangeable sodium was expressed as mmol/rat, there was a more gradual rise in the chlorothiazide-treated animals, in accordance with their slower gain in weight. 8. There was no temporal association between the antihypertensive effect of chlorothiazide and changes in exchangeable sodium. 9. Thus whereas chlorothiazide treatment of spontaneously hypertensive rats slows the increase of both weight and exchangeable sodium, other mechanisms are apparently responsible for the antihypertensive action of the drug.


2016 ◽  
Vol 40 (5) ◽  
pp. 1186-1197 ◽  
Author(s):  
He Li ◽  
Xian Liu ◽  
Zhongqiao Ren ◽  
Jinxia Gu ◽  
Yingjie Lu ◽  
...  

Background/Aims: Hypertension is a major cause of stroke, and diabetes can increase incidence of this disease. We determined the role played by central angiotensin-(1-7) [Ang-(1-7)] pathway in modulating spontaneously hypertension with diabetic hyperglycemia. Methods: Western Blot analysis and ELISA were used to determine the protein expression of Ang-(1-7) and its signal pathway Mas-R-nNOS in the cerebral cortex and hippocampus of spontaneously hypertensive rats (SHR) and control animals. In a subset of animals, diabetic hyperglycemia was induced by systemic injection of streptozotocin (STZ). We analyzed a relationship between the levels of central Ang-(1-7) and plasma brain natriuretic peptide (BNP) indicating a risk of ischemic stroke. We further examined the effects of Ang-(1-7) on arterial blood pressure. Results: Our findings demonstrated for the first time that administration of STZ 1) attenuates the levels of Ang-(1-7) in the cerebral cortex and hippocampus, which are closely linked to plasma BNP; and 2) leads to downregulation of central Ang-(1-7)-Mas-R-nNOS pathways. Notably, STZ has greater effects in SHR. Additionally, inhibition of oxidative stress can largely improve downregulation of Ang-(1-7) in diabetic SHR. Moreover, central stimulation of Ang-(1-7) pathway or a blockade of oxidative stress improves systolic blood pressure in diabetic SHR. Conclusions: The Ang-(1-7) signaling pathway is engaged in the adaptive mechanisms associated with diabetic hypertension, suggesting that enhancing Ang-(1-7)-Mas-R-nNOS system is likely to be beneficial in preventing against cardiovascular and cerebrovascular dysfunction and vulnerability related to spontaneously hypertension, particularly to diabetic hypertension.


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