Stimulation of Imidazoline Receptors Inhibits Proliferation of Human Coronary Artery Vascular Smooth Muscle Cells

Hypertension ◽  
1997 ◽  
Vol 30 (2) ◽  
pp. 295-300 ◽  
Author(s):  
Soundararajan Regunathan ◽  
Donald J. Reis
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Imidazoline Receptors ◽  
Human Coronary Artery ◽  
Stimulation Of

K + Currents in Human Coronary Artery Vascular Smooth Muscle Cells

1996 ◽  
Vol 78 (4) ◽  
pp. 676-688 ◽  
Author(s):  
Maik Gollasch ◽  
Christian Ried ◽  
Rostislav Bychkov ◽  
Friedrich C. Luft ◽  
Hermann Haller
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Human Coronary Artery ◽  
K Currents

Different Migration of Vascular Smooth Muscle Cells from Human Coronary Artery Bypass Vessels

2007 ◽  
Vol 44 (2) ◽  
pp. 149-156 ◽  
Author(s):  
Sabine Weiss ◽  
Karin Frischknecht ◽  
Helen Greutert ◽  
Sravan Payeli ◽  
Jan Steffel ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Coronary Artery Bypass ◽  
Vascular Smooth Muscle Cells ◽  
Artery Bypass ◽  
Muscle Cells ◽  
Human Coronary Artery

scholarly journals A novel inhibitory effect of oxazol-5-one compounds on ROCKII signaling in human coronary artery vascular smooth muscle cells

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Abdulhameed Al-Ghabkari ◽  
Jing-Ti Deng ◽  
Paul C. McDonald ◽  
Shoukat Dedhar ◽  
Mana Alshehri ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Inhibitory Effect ◽  
Human Coronary Artery

Effects of Angiotensin II Type 2 Receptor Stimulation on Collagen Synthesis in Vascular Smooth Muscle Cells

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 709-709
Author(s):  
Mizuo Mifune ◽  
Hiroyuki Sasamura ◽  
Hideaki Nakaya ◽  
Ryoko Shimizu-Hirota ◽  
Matsuhiko Hayashi ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Collagen Synthesis ◽  
Tyrosine Phosphatase ◽  
Muscle Cells ◽  
At2 Receptor ◽  
Stimulation Of

P84 Previously, we and others have shown that angiotensin II enhances vascular smooth muscle cell extracellular matrix synthesis via stimulation of the type 1 angiotensin (AT1) receptor. Recently, expression of the type 2 (AT2) receptor has been confirmed in the adult vasculature, but its role in vascular remodeling has not yet been fully defined. In particular, conflicting data from in vivo studies have reported that AT2 receptor inhibition may either attenuate or enhance vascular hypertrophy and fibrosis. The aim of this study was to clarify the effects of direct stimulation of AT2 receptors on collagen synthesis in vascular smooth muscle cells in vitro. Firstly, retroviral gene transfer was used to supplement adult vascular smooth muscle cells with AT2 receptors to mimic the vasculature in vivo. Treatment of these cells with the AT2 receptor agonist CGP42212A (10-7 mol/L) alone did not cause a significant change in p42/p44 MAP kinase activity, but caused a modest (33%) decrease in protein tyrosine phosphatase activity. Treatment with CGP42112A also caused a dose- and time-dependent increase in both cell-associated and secretory collagen synthesis (148+17% of control at 48 h, p<0.05) which was completely inhibited by the AT2 receptor antagonist PD123319, but unaffected by the AT1 receptor antagonist losartan. The AT2 receptor-mediated stimulation of collagen synthesis was unaffected by tyrosine phosphatase inhibitors sodium orthovanadate and okadaic acid, but attenuated by pretreatment with pertussis toxin or Galphai antisense oligonuclotides. These results suggest that direct AT2 receptor stimulation can increase rather than decrease collagen synthesis in vascular smooth muscle cells, and suggest a role for Galphai in the AT2 receptor-mediated effects.

Stimulation of protein-tyrosine phosphorylation by endothelin-1 in cultured vascular smooth muscle cells

1992 ◽  
Vol 92 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Masanobu Koide ◽  
Yasuhiro Kawahara ◽  
Terutaka Tsuda ◽  
Yoshihiro Ishida ◽  
Kozui Shii ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Tyrosine Phosphorylation ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Protein Tyrosine Phosphorylation ◽  
Protein Tyrosine ◽  
Endothelin 1 ◽  
Stimulation Of

Mechanics of resting isolated single vascular smooth muscle cells from bovine coronary artery

1984 ◽  
Vol 246 (3) ◽  
pp. C277-C287 ◽  
Author(s):  
A. M. VanDijk ◽  
P. A. Wieringa ◽  
M. van der Meer ◽  
J. D. Laird
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Viscous Resistance ◽  
Resting Cells ◽  
Initial Length ◽  
Arterial Smooth Muscle

The viscoelastic behavior of single resting vascular smooth muscle cells from bovine coronary artery was studied. No maintained passive force could be recorded, even when the cells were stretched to two to four times their initial length; this finding suggests that the smooth muscle cells do not contribute to the parallel elastic component in arterial smooth muscle tissue. The force during stretch of resting arterial cells was proportional to the rate of stretch (which varied between 20 and 60% of the initial length per second). This linear viscous resistance was also found for toad stomach cells when similar stretches were applied. The stress-relaxation curves of the arterial cells could be fitted to the sum of two exponential components (with half-lives of 13.1 and 0.5 s, respectively). As a result of the above findings, a model consisting of two viscoelastic elements in parallel was proposed for a single resting arterial smooth muscle cell. The viscous resistance to stretch of resting cells in a Ca2+-containing solution was not significantly (P greater than 0.01) different from that in a Ca2+-free solution. The same result was obtained for bovine coronary arterial rings. It is concluded that an adequate model for resting arterial smooth muscle should include an intracellular viscous element.

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