The authors explored the hypothesis that prostaglandin-induced vasodilation is caused by activation of the electrogenic sodium-potassium pump which results in membrane hyperpolarization and relaxation of vascular smooth muscle. Helical strips of rat tail artery relax in response to potassium after norepinephrine-induced contractions in physiological salt solution containing a low-potassium concentration. The amplitude of this potassium-induced relaxation is used as an index of sodium-potassium ATPase activity. It was observed that PGA1, PGE2, and PGF(2α) (10-6 g/ml) significantly enhanced the magnitude of potassium-induced relaxation. PGA2 and PGE1 (10-6 g/ml) had no significant effect. PGE2 caused relaxation of contractions induced by either 25 mM KCl or norepinephrine (10-9 g/ml), and these relaxations were inhibited by 10-4 M ouabain. Indomethacin (5.3 x 10-6 g/ml) and meclofenamate (10-6 g/ml) reduced the magnitude of potassium-induced relaxation by more than 30% of control. PGF(2α) (10-5 g/ml) reversed the inhibition of potassium relaxation by meclofenamate. These observations suggest that prostaglandins induce vascular smooth muscle relaxation by stimulation of the sodium pump and that endogenous prostaglandins normally potentiate potassium relaxation.
|Original language||English (US)|
|Number of pages||7|
|State||Published - 1980|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine