Effects of epinephrine on electrical properties of Madin-Darby canine kidney cells

The present study has been performed, to test for the influence of epinephrine on the potential difference across the cell membrane (PD) of Madin-Darby canine kidney (MDCK) cells. Under control conditions, mimicking the in vivo situation, PD averages –53.3±0.9 mV (n=37). Increasing extracellular potassium concentration from 5.4 to 10 and 20 mmol/l depolarizes the cell membrane by +4.3±0.4 mV (n=5) and +15.8±1.2 mV (n=5), respectively. The application of 1 mol/l epinephrine leads to sustained hyperpolarization of the cell membrane to –71.5±0.7 mV (n=37). In the presence of epinephrine, increasing extracellular potassium concentration from 5.4 to 20 mmol/l depolarizes the cell membrane by +30.6 ±0.2 mV (n=5); 1 mmol/l barium depolarizes the cell membrane by +14.8±0.7 mV (n=20) and abolishes the effect of step increases of extracellular potassium concentration from 5.4 to 10 mmol/l. In the presence of barium, epinephrine leads to a transient hyperpolarization by –31.2 ±1.2 mV (n=18). During this transient hyperpolarization, the cell membrane is sensitive to extracellular potassium concentration despite the continued presence of barium; 10 mol/l verapamil depolarizes the cell membrane to –41.0±2.6 mV (n=11). In the presence of verapamil, the hyperpolarizing effect of epinephrine is only transient; 10 mol/l phentolamine depolarizes the cell membrane by +3.0±0.6 mV (n=8). In the presence of phentolamine, the effect of epinephrine is virtually abolished (+0.4±0.6 mV,n=8); 1 mol/l isoproterenol depolarizes the cell membrane by +2.8±0.8 mV (n=8). In the norminal absence of extracellular calcium, epinephrine leads to a transient hyperpolarization, which can only be elicited once. In conclusion, cpinephrine hyperpolarizes MDCK cells by increasing the apparent potassium conductance. This effect is transmitted by -receptors and may be mediated by increases of intracellular calcium activity.