Nimodipine inhibits the pressor activity of diaspirin-crosslinked hemoglobin (DCLHb) in the rat

Impaired nitric oxide (NO) activity is associated with an increase in blood pressure in rats. Voltage-regulated calcium channels are believed to parti cipate in this hemodynamic event. To further test this hypothesis, we exami ned the effect of nimodipine and verapamil (calcium antagonists) on the pre sser activity of diaspirin-crosslinked hemoglobin (DCLHb), a well-known NO scavenger, in anesthetized rats. Nimodipine, the most potent of the two cal cium antagonists used, was also tested against phenylephrine (alpha(1)-adre noceptor agonist). The presser effect of DCLHb was reduced markedly by nimo dipine and verapamil, whereas that elicited by phenylephrine, particularly the tonic phase of its presser response, was resistant to blockade by nimod ipine. The bradycardia and tachycardia associated with the presser effects of DCLHb and phenylephrine, respectively, were not affected by nimodipine. The presser effect elicited by DCLHb and its alteration by nimodipine were also examined in rats pretreated with 100% O-2. This treatment was found to potentiate the presser effect of DCLHb. However, this synergism did not im pair the inhibitory action of nimodipine towards the presser activity of DC LHb. Altogether these results suggest that the presser activity of DCLHb in our animal model might involve the participation of voltage-regulated calc ium channels.