Flurbiprofen, a nonsteroidal anti-inflammatory drug (NSAID), reduces bone resoφtion in periodontal disease. This therapeutic effect has been attributed to inhibition of prostaglandin synthesis. In view of the importance of carbonic anhydrase (CA) in bone resoφtion, we examined the CA-inhibitory properties of flurbiprofen using bovine and human CA II and compared them with those of acetazolamide and two other NSAIDs, ibuprofen and indometacin. Flurbiprofen inhibited both human and bovine erythrocyte CA II but to a much lesser degree than acetazolamide. Ibuprofen and indometacin were much less active in inhibiting CA II than flurbiprofen.

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We studied the action of β-adrenergic agonists on Japanese quail erythrocyte carbonic anhydrase (CA) in vitro. Earlier we had reported that epinephrine increased CA activity by 14%; the present study focused on an attempt to increase the size of this response. Washed erythrocytes from reserpine-treated (1 mg/kg daily i.m. for 3 days) and control birds were incubated for 40 min in the presence of isoproterenol 10^–6 mol/l. The activity of CA expressed as Wilbur-Anderson units/mg hemoglobin was increased by as much as 42% in reserpine-treated birds over the control depending on the conditions. Addition of 10^–5 mol/l of the β-adrenergic antagonist propranolol inhibited the isoproterenol-induced effect in nonreserpinized birds. We conclude that pretreatment with reserpine, which was accompanied by a fall in plasma catecholamine levels, particularly epinephrine levels, enhanced the activation of CA by isoproterenol.