scholarly journals PGC-1α overexpression suppresses blood pressure elevation in DOCA-salt hypertensive mice

2015 ◽  
Vol 35 (3) ◽  
Author(s):  
Qingbin Zhao ◽  
Junfang Zhang ◽  
Huifang Wang

PGC-1α over expression restores eNOS uncoupling by increasing BH4 levels and Hsp90/eNOS interaction, enhances NO generation, improves endothelium-dependently relaxation and thus lowers blood pressure. Our findings suggest that forced PGC-1α expression may be a novel strategy to prevent and treat hypertension.

2003 ◽  
Vol 142 (2) ◽  
pp. 117-122 ◽  
Author(s):  
Ludwig Patzer ◽  
Tomas Seeman ◽  
Carmen Luck ◽  
Elke Wühl ◽  
Jan Janda ◽  
...  

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Daria Golosova ◽  
Adrian Zietara ◽  
Ruslan Bohovyk ◽  
Vladislav Levchenko ◽  
Alexander Staruschenko

The extensive use of opioid-based pain management strongly correlates with poor cardiovascular and cardiorenal outcomes. Our recent studies suggest that treatment with kappa opioid receptor (KOR) agonist BRL 52537 leads to the progression of chronic kidney disease (CKD) and aggravation of salt-sensitive hypertension. We hypothesize that stimulation of KORs leads to blood pressure elevation, albuminuria, and kidney damage in healthy Sprague-Dawley (SD) rats. To characterize the effect of the KOR agonist BRL 52537 on the development of blood pressure and kidney function in vivo , SD rats were treated with a daily i.v. bolus infusion of BRL 52537 or a corresponding vehicle. To test the contribution of KOR stimulation on calcium homeostasis in podocytes, BRL 52537 was used on freshly isolated glomeruli from SD rats. Single-channel analysis was applied to assess the effect of KORs stimulation on TRPC6 channel activity in the human immortalized podocytes. Chronic treatment with BRL 52537 leads to increased mean arterial pressure (88±1 vs 101±4 mmHg, vehicle vs treated, p<0.05), podocyte basal calcium (90±12 vs 216±16 a.u., vehicle vs treated, p<0.05), and GFB impairment in SD rats which is reflected by a transient increase in albumin excretion (Alb/cre ratio 0.35±0.1 vs 0.72±0.2, vehicle vs treated, p<0.05). Cumulative probability distribution analysis of the glomerular injury score revealed a rightward shift toward a high glomerular injury score in the group treated with BRL 52537 (p<0.05). Angiotensin II level was higher in a BRL-treated group (156±17 vs 232±59 pmol, vehicle vs treated, p=0.065); however, it did not reach a statistical difference. Acute application of BRL 52537 resulted in sustained calcium response (0.23±0.01 a.u., Fluo4/FuraRed, maximum calcium response) in freshly isolated glomeruli from SD rats. Furthermore, patch-clamp experiments in human immortalized podocytes (cell-attached configuration) revealed that BRL 52537 activated TRPC6 channels. Taken together, these data support the hypothesis that administration of opioids in SD rats leads to activation of the KOR/TRPC6 pathway, which in turn led to glomerular filtration barrier impairment, increased glomerular damage, and blood pressure elevation.


Author(s):  
Baku Takahashi ◽  
Keiji Kamohara

We herein report a case of leg malperfusion caused by dynamic obstruction after aortic dissection diagnosed by the exercise ankle brachial pressure index test that could not be diagnosed solely by examining the symptoms and investigations at rest. This case suggests that exercise can be a key factor in the diagnosis of this complication. Furthermore, blood pressure elevation can be an exacerbating factor in dynamic obstruction. We recommend conducting an aggressive evaluation of the symptoms and medical examinations not only at rest but also under stress.


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