F. Rioux et al., Nimodipine inhibits the pressor activity of diaspirin-crosslinked hemoglobin (DCLHb) in the rat, CAN J PHYSL, 76(10-11), 1998, pp. 983-988
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.