The purpose of this study was to investigate the role of calcium ions in cerebrocortical vasodilatation and oxidized and reduced nicotinamide adenine dinucle otide (NAD/NADH) redox responses evoked by adenosine, anoxia, and epileptic seizures, The brain cor tex of chloralose-anaesthetized cats was treated locally with gallopamil-hydrochloride (D-600) and verapamil (Isoptin®). These organic calcium antagonists decrease the inward movement of calcium ions into vascular smooth muscle cells. Cerebrocortical vascular volume (CVV) and NADH fluorescence were measured in vivo by fluororeflectometry. Adenosine and calcium antagonists were dissolved in artificial cerebrospinal fluid (mock CSF) and applied topically to the brain cortex by superfu sion. Adenosine (10-8 to 10-3 M) resulted in con centration-dependent increases in CVV. The NADI NADH redox state was not altered below adenosine con centrations of 10" M. However, in the concentration range of 10-" to 10-3 M, significant NAD reduction was obtained. Both calcium antagonists increased CVV markedly, but did not bring about significant changes in NAD/NADH ratio and local electrical activity of the ex posed brain cortex. D-600 (2 x 106M) increased CVV as much as did 10-4 M adenosine, but it failed to diminish the vascular and metabolic effects of the adenosine. D-600 (2 x 10-4 M) resulted in an increase in CVV approximately 2.5 times greater than that caused by 10-4 M adenosine In the contraction-relaxation process in vascular smooth muscle-as a common final pathway cytoplasmic free calcium ions play a key role (Bol ton, 1979; Johansson, 1981). Decrease in calcium influx, achieved by organic calcium antagonists