Key result
Aldosterone diminishes guanylyl cyclase activity and cGMP levels in vascular smooth muscle cells by increasing oxidant stress and inducing oxidative modification of the Cys-122 residue.
Population
Bovine aortic vascular smooth muscle cells and COS-7 cells transfected with wild-type or mutant guanylyl…
Comparison
Aldosterone (10-10 mol/liter) or hydrogen peroxide vs Untreated cells or cells expressing mutant C122A…
Design
Preclinical
Authors
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Aldosterone may impair NO/cGMP vasodilation via Cys-122 oxidation; hypothesis-generating in animal models, human relevance remains untested.
Aldosterone increases oxidant stress to convert guanylyl cyclase to a nitric oxide-insensitive state via cysteinyl thiol oxidation, disrupting normal vasodilatory signaling in vascular smooth muscle cells.
Maron et al. (2009) studied Hyperaldosteronism. Aldosterone was evaluated on Guanylyl cyclase (GC) activity and cGMP levels. Aldosterone diminishes guanylyl cyclase activity and cGMP levels in vascular smooth muscle cells by increasing oxidant stress and inducing oxidative modification of the Cys-122 residue.
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