Abstract
Both natural and synthetic peroxides have been shown to enhance sympathetic neurotransmission in the bovine isolated iris (Opere et al., IOVS 37: No. 2663, 1996). Purpose. To investigate the role of intracellular calcium ([Ca++]i) in peroxide-induced potentiation of adrenergic ncurosecretion from the bovine iris. Methods. Herni-irides were isolated from bovine eyeballs and prepared for studies of field-stimulated [3H]-norepinephrine ([3H]NE) release using the supervision method. Results. Regulators of [Ca++], such as BAPTA AM (10 μM), thapsigargin (THAP, 10 MM), ruthenium red (RR, 30 μM) and oligomycin (OLIGO, 30 μM) inhibited electrically-evoked [3H]NE overflow bv 54%, 30%, 30% and 26%, lespectively. H2O2 (0.3 mM) produced a 42% increase in evoked [3H|NE release that was blocked bv RR (30 μM). Conversely, OLIGO (30 μM) potentiated H2O2 (0-3 mM)-induced enhancement of field-stimulated [3H]NE overflow bv 89%. Interestingly, both BAPTA AM (10 μM) and THAP (10 μM) had no effect on the peroxide response. Conclusions. Mitochondrial Ca++ stores are involved in H2O2,-induced potentiation of stimulated |3H]NE release. However, changes in both eytosolic and endoplasmic reticulum Ca++ stores may not affect peroxide-induced enhancement of sympathetic neurotransmission in the bovine iris.