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Characterization and cADP-Ribose Activation of Reconstituted Ryanodine Receptors from Coronary Arterial Smooth Muscle


 P144
 
 
 Recent studies indicate that cyclic ADP-ribose (cADPR) serves as a second messenger to mobilize Ca
 2+
 from sarcoplasmic reticulum (SR) independent of IP
 3
 . However, the mechanism by which cADPR activates Ca
 2+
 mobilization is poorly understood. In the present study, ryanodine receptors from SR of coronary arterial smooth muscle cells (CASMCs) were reconstituted into planar lipid bilayer. A unitary Ca
 2+
 current through this receptor/channel complex was detected at membrane potentials from -40 to +40 mV. Mean slope conductance of this current was 245 ± 4.5 pS in a symmetric cesium methanesulfonate solution. Ryanodine at 0.1-10 μM produced a typical subconductance with increased channel open probability (NP
 O
 ), and 50 μM ryanodine, however, decreased the NP
 O
 of the channels. These ryanodine effects represent a unique feature of this SR Ca
 2+
 release channel confirmed in other tissues. Addition of Ca
 2+
 into bath solution (0.01-10 μM) significantly increased the NP
 O
 of these SR Ca
 2+
 channels. cADPR significantly increased the channel NP
 0
 in a concentration-dependent manner. A 9.7-fold increase in the NP
 O
 was observed at a concentration of cADPR of 1 μM. This cADPR-induced activation of the SR Ca
 2+
 channels was completely abolished by 50 μM ryanodine. IP
 3
 had no effect on the activity of these reconstituted SR Ca
 2+
 channels even at the highest concentration studied (10 μM). It is concluded that ryanodine receptor/Ca
 2+
 channels are present in CASMCs and can be reconstituted into planar lipid bilayer. cADPR stimulates Ca
 2+
 release through the activation of ryanodine receptors on the SR of CASMCs.
