Membrane potential and excitation-contraction coupling in smooth muscle

To describe the role of the membrane potential in the regulation of the excitation-contraction coupling of smooth muscle, two types of smooth muscle tissues, the tenia coli of the guinea pig and the ear artery of the rabbit, have been compared. The first tissue provides an example of electromechanical coupling, and the second one is characterized by pharmacomechanical coupling. Under physiologic conditions tenia coli present action potentials accompanied by an entry of Ca2+ into the cells. However, the calculated amount of Ca entering during an action potential is, according to several authors, insufficient to cause contraction. An alternative mechanism to increase the intracellular Ca2+ could be a Ca-induced or depolarization-induced Ca release. Application of acetylcholine increases the ion permeability of the plasma membrane, thereby causing an increase of the spike frequency and a membrane depolarization. In addition, it induces a release of cellular Ca. However, the changes of the membrane potential seem to be the primary regulatory factor in determining the activity of this tissue. In the ear artery the role of the membrane potential seems to be much less important than in tenia coli. There is no electrical activity, and norepinephrine induces a force development without depolarizing the cells. This agonist causes a release of Ca from an intracellular store and at the same time increases the Ca permeability of the membrane. We have obtained experimental evidence suggesting that norepinephrine could act primarily on a cellular Ca store close to the cell membrane. A depletion of this store could result in a rapid flow of external Ca into this store and from there into the cytoplasm. The receptor-operated channels would be incorporated in the plasma membrane-sarcoplasmic reticulum junction.