c-Src–Dependent Nongenomic Signaling Responses to Aldosterone Are Increased in Vascular Myocytes From Spontaneously Hypertensive Rats

Aldosterone plays an important role in the pathogenesis of hypertension. We previously demonstrated that nongenomic signaling by aldosterone in vascular smooth muscle cells occurs through c-Src–dependent pathways. Here we tested the hypothesis that upregulation of c-Src by aldosterone plays a role i...

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Bibliographic Details
Published in:Hypertension (Dallas, Tex. 1979) Tex. 1979), 2005-10, Vol.46 (4, Part 2 Suppl), p.1032-1038
Main Authors: Callera, Glaucia E, Montezano, Augusto C.I, Yogi, Alvaro, Tostes, Rita C, He, Ying, Schiffrin, Ernesto L, Touyz, Rhian M
Format: Article
Language:English
Subjects:
Aldosterone - pharmacology
Animals
Arterial hypertension. Arterial hypotension
Biological and medical sciences
Blood and lymphatic vessels
Cardiology. Vascular system
Cells, Cultured
Clinical manifestations. Epidemiology. Investigative techniques. Etiology
Experimental diseases
Extracellular Signal-Regulated MAP Kinases - metabolism
Hypertension - metabolism
Male
Medical sciences
Muscle, Smooth, Vascular - metabolism
Myocytes, Smooth Muscle - metabolism
NADPH Oxidases - metabolism
p38 Mitogen-Activated Protein Kinases - metabolism
Phosphorylation - drug effects
Proline - metabolism
Proto-Oncogene Proteins pp60(c-src) - metabolism
Rats
Rats, Inbred SHR - metabolism
Rats, Inbred WKY
Signal Transduction - drug effects
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Summary:Aldosterone plays an important role in the pathogenesis of hypertension. We previously demonstrated that nongenomic signaling by aldosterone in vascular smooth muscle cells occurs through c-Src–dependent pathways. Here we tested the hypothesis that upregulation of c-Src by aldosterone plays a role in increased mitogen-activated protein (MAP) kinase activation, [H]-proline incorporation, and NADPH-driven generation of reactive oxygen species, thereby inducing cell growth, collagen production, and inflammation, respectively, in vascular smooth muscle cells from spontaneously hypertensive rats. The time course of c-Src phosphorylation by aldosterone was shifted to the left in vascular myocytes from hypertensive animals. Aldosterone rapidly increased phosphorylation of p38 MAP kinase and extracellular signal–regulated kinase with significantly greater effects in cells from spontaneously hypertensive rats versus control cells (P
ISSN:0194-911X
1524-4563
DOI:10.1161/01.HYP.0000176588.51027.35