To determine possible sources of Ca2+ during excitation-contraction coupling in smooth muscle, a vibrating Ca2+ -selective electrode was used to measure Ca2+ flux during the process of contraction. The smooth muscle model was the longitudinal muscle of the body wall of a sea cucumber Selerodactyla briareus. Because acetylcholine caused slow contractions of the muscle that were inhibited by Ca2+ channel blockers diltiazem and verapamil in earlier mechanical studies, we chose a vibrating Ca2+ -selective electrode as our method to test the hypothesis that acetylcholine may be stimulating Ca2+ influx across the sarcolemma, providing a Ca2+ source during excitation-contraction coupling. Acetylcholine treatment stimulated a net Ca2+ afflux that was both dose and time dependent. We then tested two L-type Ca2+ channel blockers, diltiazem and verapamil, and two non-specific Ca2+ blockers, cobalt (Co2+) and lanthanum (La3+) on acetylcholine- induced Ca2+ flux. All four Ca2+ blockers tested potently inhibited Ca2+ afflux induced by physiological doses of acetylcholine. We response that the acetylcholine-induced Ca2+ afflux was the result of first, Ca2+ influx through voltage-sensitive L-type Ca2+ channels, then the rapid extrusion of Ca2+ an outwardly directed carrier such as the Na Ca exchanger as suggested by Li+ substitution experiments. The vibrating Ca2+ electrode has provided new insights on the active and complex role the sarcolemma plays in Ca2+ homeostasis and regulating Ca redistribution during excitation contraction coupling.
|Original language||English (US)|
|Number of pages||8|
|Journal||Journal of Comparative Physiology - B Biochemical, Systemic, and Environmental Physiology|
|State||Published - Aug 1996|
All Science Journal Classification (ASJC) codes
- Ecology, Evolution, Behavior and Systematics
- Animal Science and Zoology