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We have studied the in vivo response of the Na+/H+ antiporter in skeletal muscle to beta 2-adrenoceptor stimulation with isoprenaline and the effect of blocking L-type calcium channels with nifedipine. Na+/H+ antiporter activity in skeletal muscle in vivo increased after beta 2-adrenoceptor stimulation with isoprenaline; nifedipine attenuated that effect. This suggests that opening of L-type calcium channels is necessary for full activation of the Na+/H+ antiporter in skeletal muscle. Bleeding also increased Na/H+ antiporter activity, which we believe could be explained by an increase in sympathetic nervous system activity as a result of hypotension. This may be one of the mechanisms by which animals under stress prepare their skeletal muscle for exercise as part of the 'fright and flight' reaction.

Original publication




Journal article


Biochim Biophys Acta

Publication Date





234 - 240


Adenosine Triphosphate, Amiloride, Animals, Calcium Channel Blockers, Calcium Channels, Carrier Proteins, Cytosol, Hydrogen-Ion Concentration, Isoproterenol, Lactates, Male, Muscle Contraction, Muscles, Nifedipine, Phosphates, Phosphocreatine, Rats, Rats, Inbred WKY, Receptors, Adrenergic, beta, Sodium-Hydrogen Exchangers