RhoA Activation in Vascular Smooth Muscle Cells from Stroke-Prone Spontaneously Hypertensive Rats
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Accession number;04A0398533
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| Title;RhoA Activation in Vascular Smooth Muscle Cells from Stroke-Prone Spontaneously Hypertensive Rats |
| Author;
MORIKI N
(Mie Univ. School Of Medicine, Tsu, Jpn)
ITO M
(Mie Univ. School Of Medicine, Tsu, Jpn)
SEKO T
(Mie Univ. School Of Medicine, Tsu, Jpn)
KUREISHI Y
(Mie Univ. School Of Medicine, Tsu, Jpn)
OKAMOTO R
(Mie Univ. School Of Medicine, Tsu, Jpn)
NAKAKUKI T
(Mie Univ. School Of Medicine, Tsu, Jpn)
KONGO M
(Mie Univ. School Of Medicine, Tsu, Jpn)
ISAKA N
(Mie Univ. School Of Medicine, Tsu, Jpn)
KAIBUCHI K
(Nagoya Univ., Nagoya, Jpn)
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Journal Title;Hypertens Res
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Journal Code:Y0303A
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ISSN:0916-9636
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VOL.27;NO.4;PAGE.263-270(2004)
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| Figure&Table&Reference;FIG.7, TBL.1, REF.44 |
| Pub. Country;Japan |
| Language;English |
| Abstract;In order to clarify a part of molecular mechanism of the activation in the title, in vitro experiments such as immunological search methods were performed using vascular smooth muscle cells from stroke-prone spontaneously hypertensive rats (SHRSP). As the result, the value of the activated RhoA in SHRSP was significantly larger than that in Wistar-Kyoto rats (WKY). There was no significant difference in the expression of RhoA/Rho kinase-related molecular group between SHRSP and WKY. Angiotensin 2 type I receptor antagonist decreased the activation of RhoA in SHRSP significantly and selectively. The expression of c-GMP dependent protein kinase I.ALPHA. (cGKI.ALPHA.) was lowered significantly in vascular smooth muscle cells of SHRSO. From the above, the possibility of decrease in expression of cGKI.ALPHA.and adjustment of autocrine/paracrine by angiotensin II was suggested as a molecular mechanism of the activation of Rhoa in vascular smooth muscle cells from SHRSP. |
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