Continuous inhibition of the renin–angiotensin system and protection from hypertensive end-organ damage by brief treatment with angiotensin II type 1 receptor blocker in stroke-prone spontaneously hypertensive rats

Life Sciences ◽  
2005 ◽  
Vol 77 (18) ◽  
pp. 2233-2245 ◽  
Author(s):  
Kumiko Takemori ◽  
Hiroyuki Ishida ◽  
Hiroyuki Ito
2007 ◽  
Vol 54 (4) ◽  
pp. 605-612 ◽  
Author(s):  
Fuki IKEDA ◽  
Kosuke AZUMA ◽  
Takeshi OGIHARA ◽  
Yukiko TOYOFUKU ◽  
Aiko OTSUKA ◽  
...  

Foods ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1571
Author(s):  
Eun-Woo Jeong ◽  
Se-Yeong Park ◽  
Yun-Sun Yang ◽  
Youjin Baek ◽  
Damin Yun ◽  
...  

Hypertension, causing cardiovascular disease, stroke, and heart failure, has been a rising health issue worldwide. Black soybeans and adzuki beans have been widely consumed throughout history due to various bioactive components. We evaluated the antihypertensive effects of black soybean and adzuki bean ethanol extracts on blood pressure, renin-angiotensin system (RAS), and aortic lesion in spontaneously hypertensive rats. A group of WKY (normal) and six groups of spontaneously hypertensive rats were administered with saline (SHR), 50 mg/kg of captopril (CAP), 250 and 500 mg/kg of black soybean extracts (BE250 and BE500), 250 and 500 mg/kg of adzuki bean extracts (AE250 and AE500) for eight weeks. BE250, BE500, AE250, and AE500 significantly (p < 0.05) reduced relative liver weight, AST, ALT, triglyceride, total cholesterol, systolic blood pressure, and angiotensin-converting-enzyme level compared to SHR. The angiotensin II level in AE500 and renin mRNA expression in BE500 and AE500 were significantly (p < 0.05) decreased compared to SHR. The lumen diameter was significantly (p < 0.05) reduced in only CAP. Furthermore, systolic and diastolic blood pressure and angiotensin II level in AE500 were lower than those of BE500. These results suggest that AE exhibit more antihypertensive potential than BE in spontaneously hypertensive rats.


1974 ◽  
Vol 48 (s2) ◽  
pp. 265s-268s ◽  
Author(s):  
D. Ganten ◽  
J. S. Hutchinson ◽  
P. Schelling

1. Angiotensin is produced by the intrinsic iso-renin-angiotensin system. 2. Angiotensin is secreted into the cerebrospinal fluid of nephrectomized rats. 3. Angiotensin in cerebrospinal fluid elevates systemic blood pressure. 4. Rats with hereditary diabetes insipidus are virtually non-responsive to intraventricular angiotensin. 5. Angiotensin II is elevated in the cerebrospinal fluid of spontaneously hypertensive rats. 6. An intraventricular perfusion of the angiotensin II receptor-blocking agent P 113 decreases blood pressure in spontaneously hypertensive rats.


2020 ◽  
Vol 9 (11) ◽  
pp. e83991110634
Author(s):  
Cassiano Costa Silva Pereira ◽  
Natália Manrique ◽  
Juliana de Moura ◽  
Gabriel Mulinari-Santos ◽  
Naara Gabriela Monteiro ◽  
...  

Hypertension is a multifactorial condition with high rates of complications such as cardiovascular and renal diseases, making it a worldwide public health concern. This disease alters calcium regulation by inducing bone loss, which is limited by anti-hypertensive drugs. One such drug, losartan, inhibits angiotensin II (Ang II) AT1 receptors. The aim of this study was to compare the process of alveolar repair in spontaneously hypertensive rats (SHR) and Wistar rats, and to assess the effect of losartan on bone dynamics. Treated and untreated rats underwent dental extraction of the upper right incisor and were euthanized 7, 14, or 28 days after surgery. Alveolar repair was then analyzed histomorphometrically and immunohistochemically by measuring proteins involved in bone metabolism. Data were analyzed using the nonparametric Kruskal-Wallis test, followed by the Mann Whitney test for comparison of samples at different times. Alveolar repair was slow in SHRs, while losartan increased bone formation and trabecular thickness in both SHRs and Wistars. Because the analyzed proteins are found in dynamic bone, it is suggested that losartan interferes with the actions of angiotensin II and the renin-angiotensin system and limits bone metabolism.


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