Jun Yamazaki (#), Tetsuro Urushidani and Taku Nagao
Department of Toxicology and Pharmacology, Faculty of Pharmaceutical Sciences, University of Tokyo, Tokyo 113, Japan (#) Present address: Department of Physiology, University of Nevada School of Medicine, Reno, Nevada 89557-0046, U.S.A.
Abstract: Ba2+ is known to pass through N-methyl-D-aspartate receptor channels and cause an increase in cGMP levels in rat cerebella. In the present study, we compared the activation of rat cerebellar nitric oxide synthase (NOS) by Ba2+ with that produced by Ca2+. Both cations stimulated L-citrulline formation in the presence of calmodulin in identical fractions eluted from an anion exchange column with a salt gradient. EC50 values for Ca2+ and Ba2+ were 200 nM and 50 microM, respectively. The IC50 of NG- monomethyl-L-arginine was the same (200 nM). These indicate a possible action of Ba2+ on NOS through the calmodulin-dependent pathway.
Barium, Nitric oxide synthase, Calmodulin
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