Effects of prostaglandin E1 on contractility and 45Ca release in rabbit aortic smooth muscle

Concentrations of prostaglandin E1 (PGE1; 10(-7) M) that do not elicit tension responses in aortic strips potentiate contractions induced by submaximal concentrations (10(-8)-10(-7) M) of norepinephrine (NE) or angiotensin III (Ang III) but not those of high K+ depolarization or maximal NE or Ang III concentrations. Higher concentrations of PGE1 (10(-6) M and above) initiate contractions which are additive with submaximal responses to NE and Ang III but not to K+. These same concentrations of PGE1 also decrease 45Ca retention at high affinity La+++-resistant sites in a manner similar to but not additive with NE and Ang III. Uptake of 45Ca at low affinity La+++-resistant sites (which is increased by high K+-depolarization) is not altered by 10(-6) M PGE1. The effects of PGE1 are not altered by decreased extracellular Ca++ (0.1 mM), decreased temperature, phentolamine or meclofenamate. Thus, PGE1 does not appear to increase uptake of extracellular Ca++ in this smooth muscle tissue. Instead, PGE1 increases mobilization of Ca++ from the same high affinity La+++-resistant sites affected by Ang III and NE and, in this manner, may increase responses to these two stimulatory agents.