scholarly journals Vascular smooth muscle cell NAD(P)H oxidase activity during the development of hypertension: Effect of angiotensin II and role of insulinlike growth factor-1 receptor transactivation

2005 ◽  
Vol 18 (1) ◽  
pp. 81-87 ◽  
Author(s):  
M CRUZADO ◽  
N RISLER ◽  
R MIATELLO ◽  
G YAO ◽  
E SCHIFFRIN ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Growth Factor ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Oxidase Activity ◽  
Receptor Transactivation

scholarly journals Protective role of vascular smooth muscle cell PPARγ in angiotensin II-induced vascular disease

2012 ◽  
Vol 97 (3) ◽  
pp. 562-570 ◽  
Author(s):  
Chiara Marchesi ◽  
Asia Rehman ◽  
Yohann Rautureau ◽  
Daniel A. Kasal ◽  
Marie Briet ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Vascular Disease ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Protective Role

Soluble klotho attenuates angiotensin II-mediated vascular smooth muscle cell ageing: role of Nrf2-antioxidant signalling

2016 ◽  
Vol 96 ◽  
pp. S25
Author(s):  
Giuseppe Maltese ◽  
Paraskevi-Maria Psefteli ◽  
Salil Srivastava ◽  
Benedetta Rizzo ◽  
Luigi Gnudi ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell

The role of the endothelium in the regulation of vascular smooth muscle cell contractions induced by angiotensin II after ischemia and reperfusion

2010 ◽  
Vol 33 (7) ◽  
pp. 1019-1024 ◽  
Author(s):  
Katarzyna Szadujkis-Szadurska ◽  
Maciej Slupski ◽  
Rafal Szadujkis-Szadurski ◽  
Leszek Szadujkis-Szadurski ◽  
Milosz Jasiñski ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Ischemia And Reperfusion

Enhanced expression of Gqα and PLC-β1 proteins contributes to vascular smooth muscle cell hypertrophy in SHR: role of endogenous angiotensin II and endothelin-1

2014 ◽  
Vol 307 (1) ◽  
pp. C97-C106 ◽  
Author(s):  
Mohammed Emehdi Atef ◽  
Madhu B. Anand-Srivastava
Keyword(s):  
Protein Synthesis ◽  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Ang Ii ◽  
Enhanced Expression

Vascular Gqα signaling has been shown to contribute to cardiac hypertrophy. In addition, angiotensin II (ANG II) was shown to induce vascular smooth muscle cell (VSMC) hypertrophy through Gqα signaling; however, the studies on the role of Gqα and PLC-β1 proteins in VSMC hypertrophy in animal model are lacking. The present study was therefore undertaken to examine the role of Gqα/PLC-β1 proteins and the signaling pathways in VSMC hypertrophy using spontaneously hypertensive rats (SHR). VSMC from 16-wk-old SHR and not from 12-wk-old SHR exhibited enhanced levels of Gqα/PLC-β1 proteins compared with age-matched Wistar-Kyoto (WKY) rats as determined by Western blotting. However, protein synthesis as determined by [3H]leucine incorporation was significantly enhanced in VSMC from both 12- and 16-wk-old SHR compared with VSMC from age-matched WKY rats. Furthermore, the knockdown of Gqα/PLC-β1 in VSMC from 16-wk-old SHR by antisense and small interfering RNA resulted in attenuation of protein synthesis. In addition, the enhanced expression of Gqα/PLC-β1 proteins, enhanced phosphorylation of ERK1/2, and enhanced protein synthesis in VSMC from SHR were attenuated by the ANG II AT1 and endothelin-1 (ET-1) ETA receptor antagonists losartan and BQ123, respectively, but not by the ETB receptor antagonist BQ788. In addition, PD98059 decreased the enhanced expression of Gqα/PLC-β1 and protein synthesis in VSMC from SHR. These results suggest that the enhanced levels of endogenous ANG II and ET-1 through the activation of AT1 and ETA receptors, respectively, and MAP kinase signaling, enhanced the expression of Gqα/PLC-β1 proteins in VSMC from 16-wk-old SHR and result in VSMC hypertrophy.

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