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.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
(5
): F509-15
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Role of 20-HETE in the impaired myogenic and TGF responses of the Af-Art of Dahl
salt-sensitive rats
#MMPMID25007877
Ge Y
; Murphy SR
; Fan F
; Williams JM
; Falck JR
; Liu R
; Roman RJ
Am J Physiol Renal Physiol
2014[Sep]; 307
(5
): F509-15
PMID25007877
show ga
The present study examined whether 20-HETE production is reduced in the renal
vasculature and whether this impairs myogenic or tubuloglomerular feedback (TGF)
responses of the afferent arteriole (Af-Art). The production of 20-HETE was 73%
lower in renal microvessels of Dahl salt-sensitive rats (SS) rats than in
SS.5(BN) rats, in which chromosome 5 from the Brown Norway (BN) rat containing
the CYP4A genes was transferred into the SS genetic background. The luminal
diameter of the Af-Art decreased by 14.7 ± 1.5% in SS.5(BN) rats when the
perfusion pressure was increased from 60 to 120 mmHg, but it remained unaltered
in SS rats. Administration of an adenosine type 1 receptor agonist (CCPA, 1 ?M)
reduced the diameter of the Af-Art in the SS.5(BN) rats by 44 ± 2%, whereas the
diameter of the Af-Art of SS rats was unaltered. Autoregulation of renal blood
flow (RBF) and glomerular capillary pressure (PGC) was significantly impaired in
SS rats but was intact in SS.5(BN) rats. Administration of a 20-HETE synthesis
inhibitor, HET0016 (1 ?M), completely blocked the myogenic and adenosine
responses in the Af-Art and autoregulation of RBF and PGC in SS.5(BN) rats, but
it had no effect in SS rats. These data indicate that a deficiency in the
formation of 20-HETE in renal microvessels impairs the reactivity of the Af-Art
of SS rats and likely contributes to the development of hypertension induced
renal injury.