A sodium transport inhibitory factor in the saliva of patients with cystic fibrosis of the pancreas.

Abstract

Extract: The saliva of patients with cystic fibrosis of the pancreas (CFP) contains higher concentrations of sodium than the saliva of normal subjects. The hypothesis that the salivary electrolyte abnormality in CFP may be due to a sodium transport inhibitory factor (or factors) present in the saliva of these patients was investigated. Such a factor would decrease sodium reabsorption in the salivary glands and cause increased sodium concentrations in the final saliva. Retrograde perfusion of the rat parotid gland was used to determine this factor. Retrograde perfusion with normal saline or saliva from normal children did not affect the rate of sodium reabsorption in the rat parotid gland. Retrograde perfusion with ouabain containing saline or saliva from patients with CFP resulted in a marked decrease of the rate of sodium reabsorption. It was concluded that saliva from patients with CFP contains a factor that causes inhibition of sodium transport in the rat parotid gland. The similarity of the effects of ouabain and saliva from patients with CFP led us to the investigation of the possibility of a common mode of action. It was demonstrated that the saliva of patients had no effect on the in vitro activity of membrane ATPase preparations obtained from beef parotid, human erythrocytes and rat kidneys. This indicates that the saliva of patients with CFP causes inhibition of sodium reabsorption in the rat parotid by an action other than inhibition of the activity of ATPase, an enzyme known to be involved in sodium transport across biological membranes. Speculation: A factor that inhibits sodium reabsorption in the rat parotid gland has been demonstrated in the saliva of patients with CFP. The same factor may be causing the salivary electrolyte abnormality of CFP. If this is true, this factor should be present in the sweat of patients with CFP since the elctrolyte abnormality is maximally expressed in the sweat glands. It is hoped that study of this factor may lead us closer to the nature of the molecular defect of CFP.