Differentiation of vasoconstrictor sensitivity caused by prostaglandin E in peripheral vascular beds of the rabbit.

The increase in perfusion pressure in the rabbit ear, hindleg and mesentery caused by close intra-arterial injection of noradrenaline (NA), and the contractile response to NA of the rabbit aortic strip were investigated with respect to their sentitivity to prostaglandin E1 (PGE1) and to the prostaglandin synthesis inhibitor indomethacin. PGE1 (100-200 ng) potentiated the increases in perfusion pressure caused by NA in the perfused hindleg and mesentery, and the contractile response to NA of the aortic strip by 25-80%, but inhibited the increase in perfusion pressure by NA in the perfused ear by 35-100%. Indomethacin (3-5 X 10(-5) M) significantly decreased the pressor responses to NA in the hindleg (by 45%) and mesentery (by 55%). This inhibitory effect by indomethacin was completely reversed by PGE1. The responses to NA in the aortic strip and the perfused ear were unaffected by indomethacin. It is concluded that the process of vasoconstriction in the vascular beds of the rabbit displays qualitative differences concerning its sensitivity to added PGE1. Furthermore, the decreased pressor responses to NA observed in some of the rabbit vascular beds after indomethacin indicate that the sensitivity to NA in these tissues in fact is increased by endogenous prostaglandin-like substances (PLS). The current results thus suggest that endogenous PLS may regulate, at a local level, the vasoconstrictor sensitivity in the rabbit systemicresistance vessels.