Contractile Effects of Prostaglandin F2α on Isolated Human Peripheral Arteries and Veins

Abstract

The effects of prostaglandin F_2α (PGF_2α, 2.8 × 10^‐7‐2.8 × 10^‐5 M) on isolated segments of human peripheral arteries and veins were investigated. In both types of vessel, PGF_2α had a concentration‐dependent contracting effect. The contraction developed more slowly and had a longer relaxation time after washing than responses induced by noradrenaline or potassium. In the veins, the maximum response to the prostaglandin was 128 ± 3.6% of that to potassium (P2α and potassium induced contractions were of similar magnitude. The arterial preparations were less responsive to PGF_2α than to noradrenaline. On a molar basis, noradrenaline was approximately 10 times more potent than PGF_2α. Veins, maximally contracted by noradrenaline or potassium, increased their tension further on addition of PGF_2α. Similarly, preparations maximally contracted by PGF_2α also showed a further increase in tension after addition of noradrenaline or potassium. The PGF_2α induced contractions were not affected by α‐adrenoceptor blockade (phentolamine, prazosin). The calcium antagonists verapamil and nifedipine relaxed preparations contracted by PGF_2α and reduced the responses in a concentration‐dependent way when added 15 min. before the prostaglandin. Immersion for 30 min. in a calcium‐free medium, reduced the PGF_2α induced response in both arteries and veins. In the veins, but not in the arteries, the responses to potassium and noradrenaline were more reduced than that to PGF_2α (P < 0.01). Contractions induced by all agents were further depressed by verapamil and nifedipine after exposing the preparations to the calcium‐free medium. It is suggested that PGF_2α induces contraction both by enhancing the transmembrane flow of calcium, and by facilitating release of calcium from intracellular stores.