SHORT-TERM TREATMENT OF STROKE-PRONE SPONTANEOUSLY HYPERTENSIVE RATS WITH AN AT1RECEPTOR BLOCKER PROTECTS AGAINST HYPERTENSIVE END-ORGAN DAMAGE BY PROLONGED INHIBITION OF THE RENIN-ANGIOTENSIN SYSTEM

2008 ◽  
Vol 35 (10) ◽  
pp. 1151-1155 ◽  
Author(s):  
Rika Hamaguchi ◽  
Kumiko Takemori ◽  
Takao Inoue ◽  
Kouichi Masuno ◽  
Hiroyuki Ito
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Renin Angiotensin System ◽  
Organ Damage ◽  
Term Treatment ◽  
Hypertensive Rats ◽  
Short Term ◽  
Short Term Treatment ◽  
Angiotensin System ◽  
Spontaneously Hypertensive ◽  
End Organ Damage

scholarly journals Short-Term Treatment with Esmolol Reverses Left Ventricular Hypertrophy in Adult Spontaneously Hypertensive Rats via Inhibition of Akt/NF-κB and NFATc4

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Begoña Quintana-Villamandos ◽  
David A. Goukassian ◽  
Sharath P. Sasi ◽  
Emilio Delgado-Baeza
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Ventricular Hypertrophy ◽  
Term Treatment ◽  
Left Ventricular ◽  
Protein Carbonyls ◽  
Hypertensive Rats ◽  
Short Term ◽  
Short Term Treatment ◽  
Spontaneously Hypertensive ◽  
Total Antioxidant

Our group has previously demonstrated that short-term treatment with esmolol reduces left ventricular hypertrophy (LVH) in spontaneously hypertensive rats (SHRs). The present study aimed to assess the molecular mechanisms related to this effect. Fourteen-month-old maleSHRswere treated intravenously with saline as vehicle (SHR) or esmolol (SHR-E) (300 μg/kg/min). Age-matched vehicle-treated male Wistar-Kyoto (WKY) rats served as controls. After 48 hours of treatment, the hearts were harvested and left ventricular tissue was separated and processed for Western blot analysis to determine the levels of Akt, NF-κB, NFATc4, Creb1, Serca2a, Erk1/2, and Sapk/Jnk. Biomarkers of oxidative stress, such as catalase, protein carbonyls, total thiols, and total antioxidant capacity were evaluated. Esmolol reversed the levels of p-NFATc4, p-Akt, and p-NF-κB in SHRs to the phospholevels of these proteins in WKY rats without modifying p-Erk1/2, p-Sapk/Jnk, p-Creb1, or Serca2a in SHR. Compared with SHR, esmolol increased catalase activity and reduced protein carbonyls without modifying total thiols or total antioxidant capacity. Short-term treatment with esmolol reverses LVH in aged SHRs by downregulation of Akt/NF-κB and NFATc4 activity. Esmolol treatment also increases catalase activity and reduces oxidative stress in SHRs with LVH.

scholarly journals Combination treatment with valsartan and amlodipine intensifies evening suppression of Bmal1 clock gene in kidneys of spontaneously hypertensive rats

2017 ◽  
Vol 64 (1) ◽  
pp. 22-25
Author(s):  
P. Potucek ◽  
M. Radik ◽  
G. Doka ◽  
E. Kralova ◽  
P. Krenek ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Clock Gene ◽  
Term Treatment ◽  
Hypertensive Rats ◽  
Short Term ◽  
Short Term Treatment ◽  
Spontaneously Hypertensive ◽  
Long Term Treatment ◽  
Significant Difference

AbstractBlood pressure (BP) rhythm is exhibited in a circadian pattern regulated by complex system of endogenous factors. Administration of pharmacological treatment at the right time can influence the efficacy of treatment; but while kidneys play significant role in BP regulation, little is known about their role in chronopharmacotherapy. This study aimed to compare differences between morning and evening dosing with valsartan and amlodipine combination in both short-term and long-term settings and to elucidate the role of kidneys in chronopharmacology. Spontaneously hypertensive rats aged between 8 and 10 weeks were daily treated with 10mg/kg of valsartan and 4 mg/kg of amlodipine, either in the morning or in the evening with treatment duration of 1 and 6 weeks. After short-term treatment, only morning treatment group demonstrated significantly better outcomes in terms of BP control when compared to placebo. After long-term treatment, both treatment groups gained superior results in BP control against placebo; however, no significant difference was seen between morning and evening treatment. Interestingly, clock gene expression in kidney has been significantly modulated only in the evening-treated groups, with treatment intensifying the reduced Bmal1 levels, while Per2 expression was less altered. However, no direct relation with the outcomes of the therapy has been observed, suggesting that pharmacotherapy may serve as an independent modulator of peripheral circadian clock in the kidney.

Renin-angiotensin system in stroke-prone spontaneously hypertensive rats

1979 ◽  
Vol 236 (3) ◽  
pp. H409-H416 ◽  
Author(s):  
M. Shibota ◽  
A. Nagaoka ◽  
A. Shino ◽  
T. Fujita
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Malignant Hypertension ◽  
Hypertensive Rats ◽  
Salt Loading ◽  
Angiotensin System ◽  
Spontaneously Hypertensive ◽  
Renin Angiotensin

The development of malignant hypertension was studied in stroke-prone spontaneously hypertensive rats (SHR) kept on 1% NaCl as drinking water. Along with salt-loading, blood pressure gradually increased and reached a severe hypertensive level (greater than 230 mmHg), which was followed by increases in urinary protein (greater than 100 (mg/250 g body wt)/day) and plasma renin concentration (PRC, from 18.9 +/- 0.1 to 51.2 +/- 19.4 (ng/ml)/h, mean +/- SD). At this stage, renal small arteries and arterioles showed severe sclerosis and fibrinoid necrosis. Stroke was observed within a week after the onset of these renal abnormalities. The dose of exogenous angiotensin II (AII) producing 30 mmHg rise in blood pressure increased with the elevation of PRC, from 22 +/- 12 to 75 +/- 36 ng/kg, which was comparable to that in rats on water. The fall of blood pressure due to an AII inhibitor, [1-sarcosine, 8-alanine]AII (10(microgram/kg)/min for 40 min) became more prominent with the increase in PRC in salt-loaded rats, but was not detected in rats on water. These findings suggest that the activation of renin-angiotensin system participates in malignant hypertension of salt-loaded stroke-prone SHR rats that show stroke signs, proteinuria, hyperreninemia, and renovascular changes.

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