Prostaglandin F(2α), but not norepinephrine, augments the maximal contractile response to potassium. To examine the mechanism underlying this augmentation, rings of canine coronary artery were studied isometrically in physiological salt solutions of various composition. The contractions evoked by prostaglandin F(2α) were larger in high-potassium, calcium-free solution than in calcium-free solution. Similar results were obtained using canine saphenous vein and femoral artery. Isoproterenol, but not nimodipine, relaxed the contractions produced by prostaglandin F(2α) in high-potassium, calcium-free solution. Unlike prostaglandin F(2α), norepinephrine failed to constrict rings in high-potassium, calcium-free solution. In calcium-free solution, prostaglandin F(2α)-induced contractions increased with increasing potassium concentrations, but no enhancement occurred when lithium was substituted for potassium. Rings of coronary artery incubated with calcium-45 did not show changes in prostaglandin F(2α)-induced calcium-45 efflux following changes in potassium concentration. These results suggest that potassium enhances coronary vascular smooth muscle contraction to prostaglandin F(2α), but not norepinephrine, independently of calcium entry.
|Original language||English (US)|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|State||Published - 1984|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)