scholarly journals Induction of B 1 -Kinin Receptors in Vascular Smooth Muscle Cells: Cellular Mechanisms of MAP Kinase Activation

Hypertension ◽  
2001 ◽  
Vol 38 (3) ◽  
pp. 602-605 ◽  
Author(s):  
Julie Christopher ◽  
Victoria Velarde ◽  
Ayad A. Jaffa
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Map Kinase ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Cellular Mechanisms ◽  
Kinase Activation ◽  
Kinin Receptors

scholarly journals Altered PDGF-BB–Induced p38 MAP Kinase Activation in Diabetic Vascular Smooth Muscle Cells

2004 ◽  
Vol 24 (11) ◽  
pp. 2095-2101 ◽  
Author(s):  
Hiroshi Yamaguchi ◽  
Masahiko Igarashi ◽  
Akihiko Hirata ◽  
Naoko Sugae ◽  
Hiromi Tsuchiya ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Map Kinase ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
P38 Map Kinase ◽  
Kinase Activation

scholarly journals RGS5 Attenuates Baseline Activity of ERK1/2 and Promotes Growth Arrest of Vascular Smooth Muscle Cells

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1748
Author(s):  
Eda Demirel ◽  
Caroline Arnold ◽  
Jaspal Garg ◽  
Marius Andreas Jäger ◽  
Carsten Sticht ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Map Kinase ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Genetic Ablation ◽  
Variable Expression ◽  
Arterial Blood

The regulator of G-protein signaling 5 (RGS5) acts as an inhibitor of Gαq/11 and Gαi/o activity in vascular smooth muscle cells (VSMCs), which regulate arterial tone and blood pressure. While RGS5 has been described as a crucial determinant regulating the VSMC responses during various vascular remodeling processes, its regulatory features in resting VSMCs and its impact on their phenotype are still under debate and were subject of this study. While Rgs5 shows a variable expression in mouse arteries, neither global nor SMC-specific genetic ablation of Rgs5 affected the baseline blood pressure yet elevated the phosphorylation level of the MAP kinase ERK1/2. Comparable results were obtained with 3D cultured resting VSMCs. In contrast, overexpression of RGS5 in 2D-cultured proliferating VSMCs promoted their resting state as evidenced by microarray-based expression profiling and attenuated the activity of Akt- and MAP kinase-related signaling cascades. Moreover, RGS5 overexpression attenuated ERK1/2 phosphorylation, VSMC proliferation, and migration, which was mimicked by selectively inhibiting Gαi/o but not Gαq/11 activity. Collectively, the heterogeneous expression of Rgs5 suggests arterial blood vessel type-specific functions in mouse VSMCs. This comprises inhibition of acute agonist-induced Gαq/11/calcium release as well as the support of a resting VSMC phenotype with low ERK1/2 activity by suppressing the activity of Gαi/o.

cAMP response of vascular smooth muscle cells to bovine parathyroid hormone

1984 ◽  
Vol 247 (6) ◽  
pp. E822-E826 ◽  
Author(s):  
R. C. Stanton ◽  
S. B. Plant ◽  
D. A. McCarron
Keyword(s):  
Smooth Muscle ◽  
Parathyroid Hormone ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Base Line ◽  
Cellular Mechanisms ◽  
Smooth Muscle Tissue ◽  
Camp Content

Parathyroid hormone (PTH) is a vasodilator of vascular smooth muscle tissue. It has been shown to produce this vasodilation in normotensive and hypertensive laboratory rats. The effect is log dose dependent, maximal at 1 min and persists for 3–5 min. The cellular mechanisms involved in PTH-mediated vasodilation are unknown. In this study, we sought to determine the cellular changes of cAMP after administration of bovine (b)PTH (1–34). cAMP content of vascular smooth muscle cells was measured at 30 s, 1, 3, and 5 min after incubation with synthetic bPTH (1–34). Tissue cAMP content was decreased by 55% at 1 min (4.1 +/- 0.5 pmol/mg protein at time 0 vs. 1.9 +/- 0.2 pmol/mg protein at 1 min, P less than 0.001). After 5 min, cAMP levels returned to base-line values and increased over the next 5–10 min to levels above base line (P less than 0.01). In conclusion, our data suggest that the initial response of vascular smooth muscle cells to short-term incubation with bPTH (1–34) is an acute decrease in cAMP content.

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