Verapamil (0.17 microg kg(-1) min(-1) intravenous, i.v.) but not elgodipine (35 ng kg(-1) min(-1)) modestly enhanced the weak blood glucose increase induced by the i.v. infusion of isoprenaline (0.3 microg kg(-1) min(-1)) in conscious rabbits. However, elgodipine but not verapamil suppressed the increase in circulating insulin evoked by the agonist. Both drugs enhanced the rise in plasma lactate mediated by isoprenaline but only elgodipine potentiated the lipolytic effect of the agonist. In isolated islets elgodipine (10(-6) M) blocked forskolin (10(-6) M)-induced insulin release. However, in rabbit adipocytes elgodipine potentiated both glycerol release and cAMP accumulation induced by isoprenaline (10(-8)-10(-6) M). Excess K(+) (40-60 mM) did not alter basal lipolysis or the response to isoprenaline in either rabbit or mouse adipocytes. Therefore, Ca2+ influx through L-type Ca2+ channels does not seem to play a significant role in the lipolytic effect of isoprenaline. Metabolic alterations found with Ca2+ channel antagonists were of minor intensity and probably devoid of pathological implications.