Watanabe J, Horiguchi S, Karibe A, Keitoku M, Takeuchi M, Satoh S, Takishima T, Shirato K
First Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
Cardiovasc Res. 1994 Apr;28(4):480-4. doi: 10.1093/cvr/28.4.480.
The aim was to elucidate the functional role of the sarcoplasmic reticulum in myogenic contraction.
Small arteries which perfuse the rat gracilis muscle were isolated and cannulated. The inner diameter was measured under no flow condition. Myogenic contraction was induced by increasing transmural pressure from 40 to 100 mm Hg. The diameter transient and the steady state internal diameter were analysed at 40 (ID40) and 100 mm Hg (ID100) of lumen pressure.
In control, the vessels dilated immediately after the pressure change, and then constricted over approximately 4 min (the diameter decay). ID40 and ID100 were 120(SEM 16) and 108(12) microns (n = 6, p < 0.05), respectively. Ryanodine (10(-5) M) decreased ID40 to 82(8) microns. The relative rate of the diameter decay in the first 1 min was lower in the ryanodine treated vessels than in control, at 43(1)% v 74(7)%, n = 6 (p < 0.05). While KCl constriction was similar to that of ryanodine, the diameter decay was identical to that of control. Thus a decrease in baseline diameter was not of itself the cause of the depressed rate of diameter decay in the ryanodine treated vessels. Nisoldipine (10(-6) M) abolished myogenic contraction.
Ryanodine sensitive sarcoplasmic reticular function is probably involved in the mechanism for developing the myogenic response in rat skeletal muscle small arteries.
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