Key result
Silencing RGS-2 increases Ang II-induced Ca2+ release by ~46% in Bartter's/Gitelman's syndrome fibroblasts.
Population
Fibroblasts from six Bartter's/Gitelman's syndrome (BS/GS) patients and healthy controls
Comparison
Silencing RGS-2 by transfecting chemically… vs Not silenced cells from BS/GS patients and…
Design
Preclinical
Authors
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RGS-2 modulation of Ang II signaling remains hypothesis-generating in rare syndromes; should not change practice or guide trials.
Absolute Event Rate: 59.3% vs 40.5%
p-value: p=0.017
Silencing RGS-2 in fibroblasts from patients with Bartter's/Gitelman's syndromes restores Angiotensin II signaling, establishing RGS-2 as a key regulatory element of vascular tone in humans.
Calò et al. (2008) studied Bartter's syndrome/Gitelman's syndrome (n=6). Silencing RGS-2 vs. Not silenced cells was evaluated on Ang II-induced intracellular Ca2+ release (p=0.017). Silencing RGS-2 in fibroblasts from patients with Bartter's/Gitelman's syndromes significantly increased Ang II-induced intracellular Ca2+ release compared to not silenced cells (59.3 vs 40.5 nmol/l; P=0.017).
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