EFFECTS OF RYANODINE ON DEVELOPMENT OF MYOGENIC RESPONSE IN RAT SMALLSKELETAL-MUSCLE ARTERIES

Objective: The aim was to elucidate the functional role of the sarcopl asmic reticulum in myogenic contraction. Methods: Small arteries which perfuse the rat gracilis muscle were isolated and cannulated. The inn er diameter was measured under no flow condition. Myogenic contraction was induced by increasing transmural pressure from 40 to 100 mm Hg. T he diameter transient and the steady state internal diameter were anal ysed at 40 (ID40) and 100 mm Hg (ID100) of lumen pressure. Results: In control, the vessels dilated immediately after the pressure change, a nd then constricted over approximately 4 min (the diameter decay). ID4 0 and ID100 were 120(SEM 16) and 108(12) mu m (n = 6, p<0.05), respect ively. Ryanodine (10(-5) M) decreased ID40 to 82(8) mu m. The relative rate of the diameter decay in the first 1 min was lower in the ryanod ine treated vessels than in control, at 43(1)% nu 74(7)%, n=6 (p<0.05) . While KCl constriction was similar to that of ryanodine, the diamete r 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) abolis hed myogenic contraction. Conclusions: Ryanodine sensitive sarcoplasmi c reticular function is probably involved in the mechanism for develop ing the myogenic response in rat skeletal muscle small arteries.