Contractile effects of prostaglandin F2alpha on isolated human peripheral arteries and veins

The effects of prostaglandin F2alpha (PGF2alpha 2.8 X 10(-7) --2.8 X 10(-5) M) on isolated segments of human peripheral arteries and veins were investigated. In both types of vessel, PGF2alpha 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 (P less than 0.01); in the arteries, the maximum amplitudes of PGF2alpha and potassium induced contractions were of similar magnitude. The arterial preparations were less responsive to PGF2alpha than to noradrenaline. On a molar basis, noradrenaline was approximately 10 times more potent than PGF2alpha. Veins, maximally contracted by noradrenaline or potassium, increased their tension further on addition of PGF2alpha. Similarly, preparations maximally contracted by PGF2alpha also showed a further increase in tension after addition of noradrenaline or potassium. The PGF2alpha induced contractions were not affected by alpha-adrenoceptor blockade (phentolamine, prazosin). The calcium antagonists verapamil and nifedipine relaxed preparations contracted by PGF2alpha, 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 PGF2alpha 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 PGF2alpha (P less than 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 PGF2alpha induces contraction both by enhancing the transmembrane flow of calcium, and by facilitating release of calcium from intracellular stores.