scholarly journals Effect of chronic angiotensin-converting enzyme blockade on pressor responses to exogenous angiotensin II, noradrenaline and vasopressin in deoxycorticosterone acetate salt (DOCA)-induced hypertensive rats.

1984 ◽  
Vol 36 (2) ◽  
pp. 147-151
Author(s):  
Ee-Kiang GAN ◽  
Alias ABAS ◽  
Aishah LATIFF
Hypertension ◽  
1994 ◽  
Vol 24 (2) ◽  
pp. 195-204 ◽  
Author(s):  
S Kim ◽  
K Ohta ◽  
A Hamaguchi ◽  
T Omura ◽  
T Yukimura ◽  
...  

2020 ◽  
Vol 2020 ◽  
pp. 1-12 ◽  
Author(s):  
Peipei Feng ◽  
Zemin Wu ◽  
Hao Liu ◽  
Yafang Shen ◽  
Xu Yao ◽  
...  

Electroacupuncture (EA) can effectively alleviate anxiety disorders and memory impairments caused by various neurodegenerative diseases; however, the molecular mechanisms underlying its neuroprotective effects are unclear. Previous studies have shown that the renin-angiotensin system (RAS) comprises of two axes with mutual antagonism: the classical angiotensin converting enzyme/angiotensin II/angiotensin II type 1 receptor (ACE/Ang II/AT1R) axis and the protective angiotensin converting enzyme 2/angiotensin-(1-7)/Mas receptor (ACE2/Ang-(1-7)/MasR) axis. In this study, we observed that chronic cerebral hypoperfusion (CCH) mediated anxiety-like behavior and memory impairments in spontaneously hypertensive rats (SHR) via upregulation of the hippocampal classical axis (ACE/Ang II/AT1R) and the partial hippocampal protective axis (ACE2/Ang-(1-7)). However, Ang II levels were much higher than those of Ang-(1–7), indicating that the ACE/Ang II/AT1R axis plays a dominant role in the comorbidity of CCH and hypertension. Moreover, candesartan cilexetil (Canc) and perindopril (Peril) were used as positive control drugs. We found that EA, Canc, and Peril attenuated CCH-induced anxiety-like behavior and memory impairments in SHR, potentially via downregulation of the hippocampal classical axis (ACE/Ang II/AT1R) and upregulation of the whole hippocampal protective axis (ACE2/Ang-(1-7)/MasR). These results suggest that EA therapy for CCH with hypertension may be mediated by two hippocampal RAS axes.


Endocrinology ◽  
2006 ◽  
Vol 147 (7) ◽  
pp. 3539-3546 ◽  
Author(s):  
Walter Raasch ◽  
Christian Wittmershaus ◽  
Andreas Dendorfer ◽  
Inga Voges ◽  
Friedrich Pahlke ◽  
...  

Angiotensin II type 1 (AT1) receptors are expressed within organs of the hypothalamo-pituitary-adrenal (HPA) axis and seem to be important for its stress responsiveness. Secretion of CRH, ACTH, and corticosterone (CORT) is increased by stimulation of AT1 receptors. In the present study, we tested whether a blockade of the angiotensin II system attenuates the HPA axis reactivity in spontaneously hypertensive rats. Spontaneously hypertensive rats were treated with candesartan (2 mg/kg), ramipril (1 mg/kg), or mibefradil (12 mg/kg) for 5 wk. In addition to baseline levels, CORT and ACTH responses to injection of CRH (100 μg/kg) were monitored over 4 h. mRNA of CRH, proopiomelanocortin, AT1A, AT1B, and AT2 receptors was quantified by real-time PCR. All treatments induced equivalent reductions of blood pressure and had no effect on baseline levels of CORT and ACTH. However, both candesartan and ramipril significantly reduced CRH-stimulated plasma levels of ACTH (−26 and −15%) and CORT (−36 and −18%) and lowered hypothalamic CRH mRNA (−25 and −29%). Mibefradil did not affect any of these parameters. Gene expression of AT1A, AT1B, and AT2 receptors within the HPA axis was not altered by any drug. We show for the first time that antihypertensive treatment by inhibition of AT1 receptors or angiotensin-converting enzyme attenuates HPA axis reactivity independently of blood pressure reduction. This action is solely evident after CRH stimulation but not under baseline conditions. Both a reduced pituitary sensitivity to CRH and a down-regulation of hypothalamic CRH expression have the potential to reduce HPA axis activity during chronic AT1 blockade or angiotensin-converting enzyme inhibition.


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