The myocardium of molluscs exhibits profound anoxia tolerance, however the cellular mechanisms underlying heart performance during normoxia and anoxia are not well understood. In the present study we investigated the role of the sarcoplasmic reticulum (SR) during normoxia and chemical anoxia (2 mM sodium cyanide) in electrically paced ventricle preparations from the common cockle (Cerastoderma edule) at ~19°C. Acute anoxia caused a substantial increase in resting tension but did not significantly affect the force of contraction, rate of contraction or rate of relaxation in myocardial preparations. SR inhibition (ryanodine, 10 µM; thapsigargin, 2 µM) attenuated the increase in resting tension, and also caused a significant decrease in the force of contraction during anoxia. During normoxia, SR inhibition reduced the force and rate of contraction by 20-30 % at contraction frequencies of 0.2 Hz and 0.5 Hz. SR inhibition also elicited an increase in resting tension at 0.5 Hz. Our results suggest that the SR plays a role in maintaining cardiac performance during anoxia in cockle myocardium. Furthermore, the SR is operative during normoxia and is relatively more important in the cockle heart than in many ectothermic vertebrates. As efforts to understand the evolution of the SR are advanced, anoxia tolerant invertebrates may serve as valuable model organisms.
Drivers of growth in a keystone fished species along the European Atlantic coast: The common cockle Cerastoderma edule
