The influence of the divalent cations, Ca2+, Mg2+ and Ba2+, on the contractile response of the rat aorta to KCl and on the recovery of this response after nifedipine treatment was analyzed. KCl (80 mmol/l) promoted a two-phase (phasic and tonic) contractile response in Krebs solution but, as expected, no contractile response in Ca2+-free medium. In Mg2+-free medium, the phasic response to KCl was unaffected but the tonic one decreased slowly, suggesting that a long incubation time in the absence of Mg2+ (65 min) promotes a loss of or a change in the intracellular distribution of this ion that modifies Ca2+ entry through L channels or Ca2+ handling. Ba2+ (1.8 mmol/l) contracted the rat aorta in the absence or presence of Ca2+ but, when Ca2+ was not present, Ba2+ modified the contractile process so that a new addition of KCl did not reproduce the contractile response. After nifedipine treatment, no phasic response to KCl was observed and only a slow response appeared that increased as long as the KCl was present (45 min). After washing, KCl induced a phasic response similar to the standard response, but a smaller tonic one. Divalent cations accelerated the recovery of the channels involved in the tonic contraction. However, the recovery of the Ca2+ channels related to the phasic contraction was independent of divalent cations.

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