FACTORS CONTROLLING CHANGES IN INTRACELLULAR CA2-ARTERY SMOOTH-MUSCLECELLS( CONCENTRATION PRODUCED BY NORADRENALINE IN RAT MESENTERIC)

1. The intracellular Ca2+ concentration ([Ca2+](i)) was measured in me senteric artery smooth muscle cells using the fluorescent indicator in do-1. 2. Noradrenaline (1-10 mu M) produced a transient increase in [C a2+](i). This response was unaffected by the removal of external calci um suggesting that the bulk of the increase in [Ca2+](i) produced by n oradrenaline is due to release from an intracellular store. 3. The mai ntained application of caffeine (10 mM) produced a transient rise in [ Ca2+](i). The rate of relaxation was slower than that of the noradrena line response. If caffeine was removed at the peak of the rise in [Ca2 +](i) then [Ca2+](i) recovered more quickly than was the case in both the maintained response to noradrenaline and that to caffeine. 4. In t he presence of noradrenaline, caffeine or thapsigargin elevated [Ca2+] (i). However, if thapsigargin or caffeine was added first, the subsequ ent application of noradrenaline did not increase [Ca2+](i), suggestin g that only part of the caffeine-sensitive store is sensitive to norad renaline. 5. The recovery of [Ca2+](i) during the application of caffe ine was unaffected by the removal of external sodium suggesting that N a+-Ca2+ exchange is not important in the reduction in [Ca2+](i). The a ddition of lanthanum (1 mM) did, however, greatly slow [Ca2+](i) recov ery. 6. We conclude that the three major factors responsible for remov ing Ca2+ ions from the cytoplasm are: (i) a caffeine- and noradrenalin e-sensitive store (43 %), (ii) a caffeine sensitive but noradrenaline- insensitive store (36 %), and () a sarcolemmal Ca2+-ATPase (iii) (16 % ). Finally, a 5 % contribution remains to be accounted for.