Maternal high-salt diet altered PKC/MLC20 pathway and increased ANG II receptor-mediated vasoconstriction in adult male rat offspring

2016 ◽  
Vol 60 (7) ◽  
pp. 1684-1694 ◽  
Author(s):  
Weisheng Li ◽  
Juanxiu Lv ◽  
Jue Wu ◽  
Xiuwen Zhou ◽  
Lin Jiang ◽  
...  
2018 ◽  
Vol 5 ◽  
Author(s):  
Stephanie A. Segovia ◽  
Mark H. Vickers ◽  
Claudia J. Harrison ◽  
Rachna Patel ◽  
Clint Gray ◽  
...  

2014 ◽  
Vol 76 (1) ◽  
pp. 17-23 ◽  
Author(s):  
Erin K. Zinkhan ◽  
Brook Y. Lang ◽  
Baifeng Yu ◽  
Yan Wang ◽  
Chengshe Jiang ◽  
...  

2021 ◽  
pp. 108751
Author(s):  
Rodrigo Moraga-Amaro ◽  
Raul Díaz-Galarce ◽  
Juan P. Donoso-Ramos ◽  
Valentina Ugalde ◽  
Sergio Linsambarth ◽  
...  

2002 ◽  
Vol 283 (1) ◽  
pp. R243-R248 ◽  
Author(s):  
Jennifer M. Sasser ◽  
Jennifer S. Pollock ◽  
David M. Pollock

To determine the influence of chronic ANG II infusion on urinary, plasma, and renal tissue levels of immunoreactive endothelin (ET), ANG II (65 ng/min) or saline vehicle was delivered via osmotic minipump in male Sprague-Dawley rats given either a high-salt diet (10% NaCl) or normal-salt diet (0.8% NaCl). High-salt diet alone caused a slight but not statistically significant increase (7 ± 1%) in mean arterial pressure (MAP). MAP was significantly increased in ANG II-infused rats (41 ± 10%), and the increase in MAP was significantly greater in ANG II rats given a high-salt diet (59 ± 1%) compared with the increase observed in rats given a high-salt diet alone or ANG II infusion and normal-salt diet. After a 2-wk treatment, urinary excretion of immunoreactive ET was significantly increased by ∼50% in ANG II-infused animals and by over 250% in rats on high-salt diet, with or without ANG II infusion. ANG II infusion combined with high-salt diet significantly increased immunoreactive ET content in the cortex and outer medulla, but this effect was not observed in other groups. In contrast, high-salt diet, with or without ANG II infusion, significantly decreased immunoreactive ET content within the inner medulla. These data indicate that chronic elevations in ANG II levels and sodium intake differentially affect ET levels within the kidney and provide further support for the hypothesis that the hypertensive effects of ANG II may be due to interaction with the renal ET system.


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