Mechanism of membrane stabilization by calcium in vascular smooth muscle

1978 ◽  
Vol 235 (5) ◽  
pp. C227-C232 ◽  
Author(s):  
R. C. Webb ◽  
D. F. Bohr

In this study we observed relaxation in helical strips of rat tail artery in response to high concentrations of calcium after contraction induced by 10(-7) g/ml norepinephrine. This action of calcium on vascular smooth muscle contraction is referred to as the “membrane-stabilizing effect” of calcium. The current study demonstrates that changes caused by many of the variables that alter this relaxation induced by calcium parallel changes in relaxation in response to potassium; both are attenuated by ouabain, low sodium, reduced temperature, and low potassium. Relaxation produced by manganese is not similarly affected. Because potassium has been shown to cause relaxation of vascular smooth muscle by increasing the activity of sodium-potassium ATPase, we conclude that the relaxation produced by high concentrations of calcium is dependent on the activity of sodium-potassium ATPase; that produced by manganese is not.

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

1991 ◽  
Vol 205 (2) ◽  
pp. 199-202 ◽  
Author(s):  
Shinjoh Masayoshi ◽  
Nakaki Toshio ◽  
Otsuka Yukari ◽  
Sasakawa Nobuyuki ◽  
Kato Ryuichi

1994 ◽  
Vol 266 (3) ◽  
pp. H898-H902 ◽  
Author(s):  
F. Ohkawa ◽  
U. Ikeda ◽  
K. Kawasaki ◽  
E. Kusano ◽  
M. Igarashi ◽  
...  

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.


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