Key result
Ablation of the TRPV1 gene exacerbated renal damage induced by DOCA-salt hypertension in mice, indicating a protective role for TRPV1 against hypertension-induced end-organ damage.
Why the study?
Does deletion of TRPV1 receptors exacerbate renal damage in mice with DOCA-salt induced hypertension?
Population
Wild-type (WT) and TRPV1-null mutant (TRPV1-/-) mice
Comparison
Hypertension induced by uninephrectomy and… vs Vehicle-treated WT and TRPV1-/- mice
Design
Preclinical
Follow-up
4 treatment weeks
Authors
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Should not change clinical practice in hypertension; leaves open TRPV1 as a target for renal protection research.
Does deletion of TRPV1 receptors exacerbate renal damage in mice with DOCA-salt induced hypertension?
TRPV1 receptors may provide a protective mechanism against end-organ renal damage induced by hypertension.
Wang et al. (2008) studied Hypertension-induced renal damage. TRPV1 gene ablation (TRPV1-/- mutant) vs. Wild-type (WT) mice was evaluated on Renal damage (urinary excretion of albumin and 8-isoprostane, glomerulosclerosis, tubulointerstitial injury, fibrosis, and macrophage infiltration). Ablation of the TRPV1 gene exacerbated renal damage induced by DOCA-salt hypertension in mice, indicating a protective role for TRPV1 against hypertension-induced end-organ damage.
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