Source of calcium for contractile responses of large and small human intramyometrial arteries

The role of calcium (Ca2+) released from intracellular stores and the entry of extracellular Ca2+ for vasopressin (AVP)-induced responses in large and small, human, intramyometrial arteries was investigated. There was no stat istical difference as revealed by pD(2) values (-log EC50), in the sensitiv ity of large and small vessels to AVP, Nimodipine caused an inhibition of c ontractions induced by low concentrations (10(-10) mol/l) of AVP in both ty pes of vessels but, at higher concentration (>10(-10) mol/l), whereas respo nses in small arteries were diminished, in large arteries they remained unc hanged, In Ca2+-free solution, responses of large and small arteries to pot assium and to 10(-10) mol/l AVP were abolished. With 10(-6) mol/l AVP, resp onse in small arteries was completely inhibited, whereas in large arteries it was reduced by similar to 50%, Additional experiments were done on large arteries. Thapsigargin (TSG), which causes depletion of internal Ca2+ stor es, caused a significant reduction in responses. Following treatment with T SG, responses to AVP in Ca2+-free solution were almost completely inhibited but arteries responded again when incubated in normal physiological salt s olution. The results indicate that in contrast to large arteries, small art eries are highly dependent on extracellular Ca2+ Response of large arteries showed considerable dependence on Ca2+ stored internally particularly, for maximum activation.