ABSTRACT
AIM: To investigate the changes of G?q/11 and phospholipase C(PLC) of the aorta and to evaluate the role of signal transduction pathway mediated by G?q/11 in the pathogenesis of spontaneous hypertension. METHODS: Blood pressure was measured by intubation of carotid, and the level of plasma angiotension Ⅱ was measured by radioimmunoassay. In addition, G?q/11 and PLC contents in aorta were determined by Western blot analysis. RESULTS: Arterial blood pressure was not changed in 4-week-old spontaneously hypertensive rats(SHR), but it was increased markedly in 12-week-old SHR. The G?q/11 expression of aorta in 4-week-old SHR was increased by 69 2%( P
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AIM: To investigate the crosstalk between angiotensin Ⅱ (AngⅡ)-mediated and platelet-derived growth factor (PDGF)-mediated signal transduction in vascular smooth muscle proliferation.METHODS: A model of renal hypertension was made by two kidney/one-clip operation. Level of PDGF receptor ? subunit of aorta was measured by Western Blot analysis. The effect of Ang Ⅱ on PDGF receptor ? subunit expression was investigated in culture rat aortic vascular smooth muscle cells (VSMC).RESULTS: Systolic blood pressure obviously increased at 8th week after operation, whereas the level of PDGF receptor ? subunit of aorta significantly increased by 126.6% ( P
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AIM: To investigate the role of G?q/11-mediated signal transduction pathway in cardiac hypertrophy induced by angiotensin II (AngII). METHODS: Renal hypertension was performed by placing a sliver clip around the left renal artery(2K1C). Hemodynamic parameters, the ratio of left ventricular weight to body weight, the AngII contents and the activities of phospholipase C (PLC) in myocardium were measured at 1st, 2nd, 4th and 8th week after operation, respectively. The levels of G?q/11 were assayed by Western blot analysis. -leucine incorporation and levels of G?q/11 were measured in cultured neonatal rats ventricular myocyte after AngII stimulation. RESULTS: In 2K1C group, blood pressure and the ratio of left ventricle of heart to body weight were significantly increased compared with sham group between 2nd to 8th week. AngII content increased from 1st to 8th week after operation. Compared with the sham group, levels of G?q/11 in 2K1C group increased by 25.0% and 35.8% at 4th and 8th week( P
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AIM: To investigate the effect of heme oxygenase on vascular remodeling in renal hypertension. METHODS: Male Wistar rats were randomly divided into sham-operated, 2K1C (two-kidney one-clip) and hemin-induced groups. Four weeks after the treatments, the thickness of aortic media and HO enzymatic activity of the aorta were determined. Immunohistochemical staining was carried out to detect protein of HO-1 in the aorta. RESULTS: The blood pressure in 2K1C renal hypertension rats started to increase two weeks after the surgery and stabled at a high level at the 4th week. Hemin, an inducer of HO-1, markedly inhibited the increase in blood pressure. Aortic medium thickness of the 2K1C rats at 4th week was 27 5% thicker than that in the sham-operated rats. The thickness of aortic medium of the hemin-induced rats was 16 1% less than that in 2K1C group. At the 4th week after operation, protein level and enzymatic activity of HO-1 in aorta were higher than that in 2K1C group compared to those in the sham-operated group. CONCLUSION: Renal hypertension caused vascular remodeling and the activation of HO-1. HO-1 induction decreased the blood pressure of renal hypertension and reduced vascular remodeling.