Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\25298524
.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Am+J+Physiol+Renal+Physiol
2014 ; 307
(12
): F1355-62
Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Serelaxin reduces oxidative stress and asymmetric dimethylarginine in angiotensin
II-induced hypertension
#MMPMID25298524
Sasser JM
; Cunningham MW Jr
; Baylis C
Am J Physiol Renal Physiol
2014[Dec]; 307
(12
): F1355-62
PMID25298524
show ga
Recent findings suggest the therapeutic action of relaxin during hypertension is
dependent on nitric oxide synthase (NOS) activation; however, the mechanisms
underlying the beneficial effects of relaxin on the NOS system have not been
fully elucidated. We hypothesized that the protective effects of relaxin include
reducing both oxidative stress and the endogenous NOS inhibitor asymmetric
dimethylarginine (ADMA). We examined the effect of Serelaxin [human recombinant
relaxin-2 (RLX)] in male Sprague-Dawley rats given high-dose angiotensin (ANG) II
(400 ng·kg(-1)·min(-1) sc) for 6 wk or shams. RLX was administered (4 ?g/h sc) to
half of the rats in each group after 2 wk of ANG II for the remaining 4 wk. ANG
II induced hypertension and proteinuria, reduced NO oxidation products (NOx), and
increased oxidative stress (NADPH oxidase activity, thiobarbituric acid-reactive
substances, and 8-isoprostane excretion) and plasma ADMA. While RLX had no effect
on sham rats, RLX attenuated the ANG II-dependent hypertension (165 ± 5 vs. 135 ±
13 mmHg, P < 0.05) and proteinuria at 6 wk (62 ± 6 vs. 41 ± 4 mg·day(-1)·100
g(-1), P < 0.05) and normalized oxidative stress and circulating ADMA, in
association with restored NOx excretion and kidney cortex NOx. We found that RLX
had no impact on the ADMA-regulatory enzymes protein arginine methyltransferase
and dimethylarginine-dimethylaminohydrolase (DDAH). Furthermore, RLX treatment
did not increase DDAH activity in kidney cortex or liver. These data suggest that
benefits of RLX treatment include reduced ADMA levels and increased NO
bioavailability, possibly due to its antioxidant effects.