The purpose of this study was undertaken to test if alteration of calcium flux across the sarcolemma or sarcoplasmic reticulum change subsequent relaxation of rat aorta in tissue model of ischemia. Thoracic aorta ring segments(2-3mm wide) were studied with solution that mimicked real ischemia condition(hypoxia, acidosis, elevated lactate levels and zero sub strate). During ischemic condition, the effect of treatments thought to decrease cytosolic cal cium were tested. Half time(t(1/2)) and degree of stabilized relaxation were 2.4+/-0.9 minutes and 17.6+/-12.1%(NE 10-7 M precontraction as 100%) for verapamil(10-6 M), 3.3+/-0.7 min- utes, 22.2+/-3.9% for low Ca2+(0.75mM) in ischemic solution. Interventions aimed to elevat- ing cytosolic calcium were also tested. 3.8+/-0.9 minutes and 68.6+/-8.1% for high (10.0 mM) Ca2+ in ischemic solution, 3.7+/-0.7 minutes, 72.8+/-3.9/. for ryanodine(3X10-9 M). 3.8+/-0.5 minutes, 53.4+/-2.6% for isoproterenol. Without any treatment or agents during ischemia, hlaf time and degree of relaxation were 4.0+/-1.7 minutes, 74.6+/-13.2%, enothelium and time independent. These data support that treatment or agent thought to reduce influx of cytosolic calcium levels exaggerated the severity of relaxation. The mechanism of relaxation in ischsmia is not completely clear, but it is suggested that a reduction of calcium influx may involved and directly related.