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Vol. 59, Issue 1, 104-112, January 2001
Departments of Physiology (G.T., M.G., S.L.-O., M.R.-P.),
Biochemistry (M.d.C.B.-A., E.A.), and Medicine (D.R.-P.), Alcalá
University; Nephrology Section, Hospital Príncipe de Asturias
(D.R.-P.), and Instituto Reina Sofía de Asturias (D.R.-P.), and
Instituto Reina Sofía de Investigaciones Nefrológicas,
Madrid, Spain; Novartis Pharma Laboratories, Basel, Switzerland (J.M.);
and Research Unit, Hospital de Guadalajara, Spain (T.P.)
In the last years, reactive oxygen species (ROS) have been proposed as
mediators of proliferative/hypertrophic responses to angiotensin II
(Ang II), both in vivo and in vitro. However, the hypothesis that the
Ang II-dependent cell contraction could be mediated by ROS,
particularly H2O2, has not been tested. Present experiments were devoted to test this hypothesis and to analyze the
possible mechanisms involved. Catalase (CAT) prevented the increased
myosin light chain phosphorylation and the decreased planar cell
surface area (PCSA) induced by 1 µM Ang II in cultured rat vascular
smooth muscle cells (VSMC). This preventive effect of CAT was also
detected when 1 µM platelet-activating factor (PAF) was used as a
contractile agonist instead of Ang II. Similar results were found when
using horseradish peroxidase as an H2O2 scavenger or cultured rat mesangial cells. In vascular smooth muscle
cells, CAT modified neither the binding of labeled Ang II nor the Ang
II-induced inositol 1,4,5-trisphosphate (IP3) synthesis. However, it completely abolished the Ang II-dependent calcium peak, in
a dose-dependent fashion. CAT-loaded cells (increased intracellular CAT
concentration over 3-fold) did not show either a decreased PCSA or an
increased intracellular calcium concentration after Ang II treatment.
Ang II stimulated the H2O2 synthesis by cultured cells, and the presence of CAT in the extracellular
compartment significantly diminished the Ang II-dependent increased
intracellular H2O2 concentration. The
physiological importance of these findings was tested in rat thoracic
aortic rings: CAT prevented the contraction elicited by Ang II. In
summary, present experiments point to H2O2 as a
critical intracellular metabolite in the regulation of cell contraction.
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