The role of superficial SR in modulating force development induced by Ca entry into arterial smooth muscle.
Evidence is presented for the hypothesis that the superficial sarcoplasmic reticulum (SR) of arterial smooth muscle functions as a "regulated buffer barrier" to Ca entry into the bulk of the myoplasm. Depletion of the intracellular Ca pool, which is sensitive to both norepinephrine (NE) and caffeine, decreases subsequent contraction due to high K+ depolarization. This effect is due to enhanced Ca accumulation by the SR, since it is not accompanied by a decrease in 45Ca influx. Using the Ca entry blockers D600 and La3+ to reduce tension and Ca influx during activation by NE and high K+ depolarization, we observed a threshold type of tension dependence on Ca influx. During the tonic contractile phases, the Ca influx threshold for NE-induced tension was much lower than that for high K+-increased tension. 10(-7) M NE, which discharged the SR by only 15%, caused a much smaller decrease in the Ca influx threshold for contraction, indicating that the degree of SR discharge is related to the depression of the threshold. Inositol-trisphosphate was shown to be capable of rapidly discharging Ca2+ from the SR in skinned arterial smooth muscle cells.
D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D002110:Caffeine / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000378:metabolism*; D009638:Norepinephrine / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D012519:Sarcoplasmic Reticulum / Q000502:physiology*
D002110:Caffeine; D011188:Potassium; D002118:Calcium; D009638:Norepinephrine