Differences in contractile activation between human myometrium and intramyometrial arteries

Small intramyometrial arteries and pieces of adjacent myometrial tissue were obtained from 25 non-pregnant women undergoing hysterectomy. Vascular and myometrial preparations were dissected, mounted in organ baths and isometric tension was recorded. Myometrial strips, but no vascular preparation, developed spontaneous contractile activity. Noradrenaline (NA) and vasopressin (VP) contracted both vessels and myometrium. Prostaglandin F2 alpha (PGF 2 alpha) contracted the myometrial tissue, but had only a minor effect on the vessels. Removal of extracellular calcium almost abolished the myometrial responses to high K+ (124 mM)-solution, PGF 2 alpha, NA and VP. The vascular responses remaining after this treatment were 18% (K+), 34% (NA) and 25% (VP) of control contractions induced by high K+ (124 mM). Nifedipine potently depressed myometrial contractions induced by NA and VP, but was less active against the vascular responses to these agents. In preparations exposed to calcium-free medium, nifedipine (10(-7) M) almost abolished myometrial contractions induced by calcium in the presence of K+ (124 mM), NA or VP. It also effectively depressed vascular responses to calcium in the presence of K+, but was less active if NA and VP were present. It is suggested that PGF2 alpha has almost no contractant effect on intramyometrial arteries, and that the activation process in these vessels is much less dependent on extracellular calcium than that of the myometrium.