Having previously found that in vivo administration of norepinephrine (NE) depolarizes the membrane of hamster sartorius muscle cells, the present study evaluated NE effects in vitro where alterations in blood flow were eliminated. Muscles were submerged in a temperature-controlled chamber, held at their resting length, and impaled with glass microelectrodes. Norepinephrine addition (maximum concentration of 10-20 μM at the muscle surface) induced significant depolarization in sartorius muscle cells and significant hyperpolarization in soleus muscle cells (P < 0.05). Ascorbic acid (final concentration 15-25 μM), the vehicle for NE, evoked no significant alteration in resting membrane potentials of either muscle. Isoproterenol, a β-adrenoceptor agonist, elicited responses similar to those of NE; phenylephrine, an α-adrenoceptor agonist, had no significant effect. The data suggest that the NE response is mediated through the β-adrenergic pathway and that in the hamster, both hyperpolarization and depolarization can be observed under the same experimental conditions, depending on the muscle in question.
- Membrane potential
- Skeletal muscle
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience