The effects of prostaglandin (PGF2α) on the contractility of vascular smooth muscle were investigated in the helical strip of the rabbit aorta. The aortic strip was immersed in the phosphate-buffered Tyrode s solution which was equilibrated with 100% O_{2} at 35℃ and its isometric tension was measured. The contraction was induced by (PGF2α), norepinephrine (NE), or potassium (40 mM) in the nomal Tyrode s solution (1 mM, Ca2+) or Ca2+-free Tyrode s solution. Effects of verapamil and phentolamine on the contraction were also observed. The aortic strip began to contract at the concentration of 5 μg% and reached the maximal contraction at the concentration of 150 μg% (PGF2α). The maximal contraction was corresponded respectively to 52.2±3.0% and 81.5±3.5% of maximal contraction by NE (1 X 10-5M) and 40 mM K+. And the maximal contractions by (PGF2α) or NE were induced at the concentration of about 1 mM Ca2+. (PGF2α) induced the contraction of aortic strip even after induction of contraction by 40 mM K+ and the contraction by (PGF2α) was not blocked by the α-receptor blocker, phentolamine. And the contraction by the (PGF2α) was inhibited partially by a verapamil at the concentration of 1 X 10-5M and the contraction began to increase at the concentration of 1 X 10-4M verapamil. Whereas the contraction by NE was completely blocked by verapamil. Though both the (PGF2α) and NE induced the contraction in the Ca2+-free Tyrode s solution, the peak tension was not maintained. But the rate of tension decline was lower in the contraction by (PGF2α) than in that by NE. The verapamil did not inhibit the contraction by (PGF2α) in the Ca2+-free Tyrode s solution and increased the contraction at the concentration of above 1 X 10-4M. The NE-induced contraction in the Ca2+-free Tyrode s solution was inhibited completely by a verapamil. From the above results it is suggested that the contraction induced by (PGF2α) results from the promotion of the both Ca2+ influx and the intracellular Ca2+ release by different way from NE.
