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2015 ; 10
(7
): e0132594
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Regulation of Renal Hemodynamics and Function by RGS2
#MMPMID26193676
Osei-Owusu P
; Owens EA
; Jie L
; Reis JS
; Forrester SJ
; Kawai T
; Eguchi S
; Singh H
; Blumer KJ
PLoS One
2015[]; 10
(7
): e0132594
PMID26193676
show ga
Regulator of G protein signaling 2 (RGS2) controls G protein coupled receptor
(GPCR) signaling by acting as a GTPase-activating protein for heterotrimeric G
proteins. Certain Rgs2 gene mutations have been linked to human hypertension.
Renal RGS2 deficiency is sufficient to cause hypertension in mice; however, the
pathological mechanisms are unknown. Here we determined how the loss of RGS2
affects renal function. We examined renal hemodynamics and tubular function by
monitoring renal blood flow (RBF), glomerular filtration rate (GFR), epithelial
sodium channel (ENaC) expression and localization, and pressure natriuresis in
wild type (WT) and RGS2 null (RGS2-/-) mice. Pressure natriuresis was determined
by stepwise increases in renal perfusion pressure (RPP) and blood flow, or by
systemic blockade of nitric oxide synthase with L-NG-Nitroarginine methyl ester
(L-NAME). Baseline GFR was markedly decreased in RGS2-/- mice compared to WT
controls (5.0 ± 0.8 vs. 2.5 ± 0.1 ?l/min/g body weight, p<0.01). RBF was reduced
(35.4 ± 3.6 vs. 29.1 ± 2.1 ?l/min/g body weight, p=0.08) while renal vascular
resistance (RVR; 2.1 ± 0.2 vs. 3.0 ± 0.2 mmHg/?l/min/g body weight, p<0.01) was
elevated in RGS2-/- compared to WT mice. RGS2 deficiency caused decreased
sensitivity and magnitude of changes in RVR and RBF after a step increase in RPP.
The acute pressure-natriuresis curve was shifted rightward in RGS2-/- relative to
WT mice. Sodium excretion rate following increased RPP by L-NAME was markedly
decreased in RGS2-/- mice and accompanied by increased translocation of ENaC to
the luminal wall. We conclude that RGS2 deficiency impairs renal function and
autoregulation by increasing renal vascular resistance and reducing renal blood
flow. These changes impair renal sodium handling by favoring sodium retention.
The findings provide a new line of evidence for renal dysfunction as a primary
cause of hypertension.
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