Effects of Insulin on Vascular Smooth Muscle Contraction

1996 ◽  
pp. 215-223 ◽  
Author(s):  
Andrew M. Kahn ◽  
Tom Song
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Muscle Contraction ◽  
Smooth Muscle Contraction ◽  
Vascular Smooth Muscle Contraction

Calcium and Vascular Smooth Muscle Contraction

1971 ◽  
Vol 28 (5 Suppl 2) ◽  
pp. II-88-II-95 ◽  
Author(s):  
CHARLES L. SEIDEL ◽  
DAVID F. BOHR
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Muscle Contraction ◽  
Smooth Muscle Contraction ◽  
Vascular Smooth Muscle Contraction

Multiple mechanisms of vascular smooth muscle contraction

1990 ◽  
Vol 183 (2) ◽  
pp. 173-174
Author(s):  
H. Karaki ◽  
K. Sato ◽  
M. Hori ◽  
H. Ozaki ◽  
K. Sakata ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Muscle Contraction ◽  
Smooth Muscle Contraction ◽  
Vascular Smooth Muscle Contraction

Vascular smooth muscle contraction induced by Na+ channel activators, veratridine and batrachotoxin

1991 ◽  
Vol 205 (2) ◽  
pp. 199-202 ◽  
Author(s):  
Shinjoh Masayoshi ◽  
Nakaki Toshio ◽  
Otsuka Yukari ◽  
Sasakawa Nobuyuki ◽  
Kato Ryuichi
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Muscle Contraction ◽  
Smooth Muscle Contraction ◽  
Na Channel ◽  
Vascular Smooth Muscle Contraction

Inhibitory effect of interleukin-6 on vascular smooth muscle contraction

1994 ◽  
Vol 266 (3) ◽  
pp. H898-H902 ◽  
Author(s):  
F. Ohkawa ◽  
U. Ikeda ◽  
K. Kawasaki ◽  
E. Kusano ◽  
M. Igarashi ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Muscle Contraction ◽  
Interleukin 6 ◽  
Smooth Muscle Contraction ◽  
Inhibitory Effect ◽  
Sprague Dawley ◽  
Intracellular Cgmp ◽  
Dependent Relationship ◽  
Vascular Smooth Muscle Contraction

Our objective was to investigate the direct effect of interleukin-6 (IL-6) on the vascular smooth muscle contraction. We measured the contraction of endothelium-denuded aortic rings isolated from Sprague-Dawley rats. We also investigated the involvement of vasodilator prostaglandin and guanosine 3',5'-cyclic monophosphate (cGMP) productions in the effect of IL-6 using cultured rat vascular smooth muscle cells (VSMC). Exposing the aortic rings to recombinant murine IL-6 (50 U/ml) for 180 min significantly suppressed the phenylephrine (10(-9)-10(-5) M)-induced contraction. This inhibitory effect of IL-6 on the contraction tended to exhibit a dose-dependent relationship (0.5-50 U/ml). The effect of IL-6 was totally eliminated in the presence of indomethacin (10(-5) M). The release of immunoreactive 6-ketoprostaglandin F1 alpha from cultured rat VSMC was significantly increased by exposure to IL-6. Intracellular cGMP concentration in VSMC was not affected by IL-6. In conclusion, IL-6 is a potent inhibitor of the alpha-adrenergic-stimulated contraction of vascular smooth muscle. Its action is endothelium independent and mediated by the increased synthesis of prostacyclin in VSMC.

Norepinephrine and endothelin activate diacylglycerol kinases in caveolae/rafts of rat mesenteric arteries: agonist-specific role of PI3-kinase

2007 ◽  
Vol 292 (5) ◽  
pp. H2248-H2256 ◽  
Author(s):  
Christopher J. Clarke ◽  
Vasken Ohanian ◽  
Jacqueline Ohanian
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Muscle Contraction ◽  
Smooth Muscle Contraction ◽  
Pi3 Kinase ◽  
Mesenteric Arteries ◽  
Dependent Manner ◽  
Kinase Inhibition ◽  
Small Arteries ◽  
Vascular Smooth Muscle Contraction

The phosphatidylinositol (PI) signaling pathway mediates norepinephrine (NE)- and endothelin-1 (ET-1)-stimulated vascular smooth muscle contraction through an inositol-trisphosphate-induced rise in intracellular calcium and diacylglycerol (DG) activation of protein kinase C (PKC). Subsequent activation of DG kinases (DGKs) metabolizes DG to phosphatidic acid (PA), potentially regulating PKC activity. Because precise regulation and spatial restriction of the PI pathway is necessary for specificity, we have investigated whether this occurs within caveolae/rafts, specialized plasma membrane microdomains implicated in vascular smooth muscle contraction. We show that components of the PI signaling cascade-phosphatidylinositol 4,5-bisphosphate (PIP2), PA, and DGK-θ are present in caveolae/rafts prepared from rat mesenteric small arteries. Stimulation with NE or ET-1 induced [33P]PIP2 hydrolysis solely within caveolae/rafts. NE stimulated an increase in DGK activity in caveolae/rafts alone, whereas ET-1 activated DGK in caveolae/rafts and noncaveolae/rafts; however, [33P]PA increased in all fractions with both agonists. Previously, we reported that NE activated DGK-θ in a phosphatidylinositol 3-kinase (PI3-kinase)-dependent manner; here, we describe PI3-kinase-dependent DGK activation and [33P]PA production in caveolae/rafts in response to NE but not ET-1. Additionally, PKB, a potential activator of DGK-θ, translocated to caveolae/rafts in response to NE but not ET-1, and PI3-kinase inhibition prevented this. Furthermore, PI3-kinase inhibition reduced the sensitivity of contraction to NE but not ET-1. Our study shows that caveolae/rafts are major sites of vasoconstrictor hormone activation of the PI pathway in intact small arteries and suggest a link between lipid signaling events within caveolae/rafts and contraction.

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