INHIBITION OF CALCIUM-ENTRY PRESERVES CONTRACTILITY OF ARTERIAL SMOOTH-MUSCLE IN CULTURE

The addition of the growth stimulator fetal calf serum (FCS, 10%) to r ings of rat tail artery causes an increase in [Ca2+](i), accompanied b y contraction. This response was inhibited by the calcium entry blocke r verapamil (1 mu M). To investigate the effect of Ca2+ entry blockade on growth and contractility, rings of rat tail artery were cultured f or 4 days in medium with or without FCS and then mounted for tension r egistration and stimulated with noradrenaline (NA) or high-K+ solution . In cultured rings growth was quantitated by [H-3]-thymidine incorpor ation and increase in protein contents. FCS in the medium stimulated D NA synthesis by about 2-fold and increased protein contents by about 7 0%. The growth-stimulated cultured rings developed less force than fre shly prepared rings (2.2 +/- 0.3 vs. 8.3 +/- 1.0 mN/mm). The addition of 1 mu M verapamil to the medium during culture increased maximal NA- evoked force to 5.0 +/- 0.4 mN/mm but had no effect on the increases i n DNA synthesis and protein contents. Force developed by growth-arrest ed rings, cultured in the absence of FCS, was not different from that of freshly prepared rings (7.2 +/- 0.6 mN/mm). Verapamil did not affec t maximal force in these rings. Similar responses were seen when contr action was elicited by high-K+ solution. We conclude that verapamil, p resent during culture, preserves contractility of arterial smooth musc le, and that this effect is not parallel to inhibition of growth.