Key result
Loss of renal RGS2 increases mean systolic blood pressure by ~8 mmHg versus wild-type controls.
Why the study?
Does the loss of renal RGS2 cause hypertension in mice?
Does the loss of renal RGS2 cause hypertension in mice?
Absolute Event Rate: 131% vs 123%
p-value: p=0.046
Renal RGS2 plays a critical role in modulating blood pressure and preventing hypertension, highlighting the kidney's role as a final determinant of intra-arterial pressure.
Renal RGS2 loss suffices for hypertension in mice; leaves open its role as a therapeutic target in human hypertension.
G protein-coupled receptors (GPCRs) have key roles in cardiovascular regulation and are important targets for the treatment of hypertension. GTPase-activating proteins, such as RGS2, modulate downstream signaling by GPCRs. RGS2 displays regulatory selectivity for the Gαq subclass of G proteins, and mice lacking RGS2 develop hypertension through incompletely understood mechanisms. Using total body RGS2-deficient mice, we used a kidney crosstransplantation strategy to examine separately the contributions of RGS2 actions in the kidney from those in extrarenal tissues with regard to BP regulation. Loss of renal RGS2 was sufficient to cause hypertension, whereas the absence of RGS2 from all extrarenal tissues including the peripheral vasculature did not significantly alter BP. Accordingly, these results suggest that RGS2 acts within the kidney to modulate BP and prevent hypertension. These data support a critical role for the renal epithelium and/or vasculature as the final determinants of the intra-arterial pressure in hypertension.
No takes yet. Share an insight, caveat, or question.
Gurley et al. (2010) studied Hypertension (n=26). RGS2 deficiency in kidney (Kidney KO) vs. Wild-type mice transplanted with wild-type kidneys was evaluated on Mean systolic blood pressure (p=0.046). Loss of RGS2 specifically in the kidney significantly increased mean systolic blood pressure to 131 mmHg compared to 123 mmHg in wild-type controls (P=0.046).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: