Inhibition of Na+ reabsorption in the rat parotid gland by prostaglandin E1 and kallidin: implications for cystic fibrosis.

Prostaglandin E1 caused a dose-related inhibition of sodium reabsorption in the rat parotid gland when injected by retrograde perfusion into the glandular ducts. The extent of inhibition ranged from 11.7 +/- 2.4% at a dose of 2.5 micrograms to 63.8 +/- 8.9% at a dose of 31.2 micrograms. Both phospholipase A2, an enzyme involved in prostaglandin synthesis, and arachidonic acid, a precursor of prostaglandins, also increased the Na+ concentration of parotid saliva in a dose-dependent fashion. With phospholipase A2 the inhibition ranged from 21.6 +/- 4.4% at a dose of 3 micrograms to 73.5 +/- 8.2% at a dose of 30 micrograms. With arachidonic acid, the degree of inhibition was 5.1 +/- 3.0% at a 10(-5) M dose and 57.7 +/- 10.2% at a dose of 10(-3) M. Lysine bradykinin (kallidin), a peptide present in salivary and other exocrine glands and their secretions, also caused a 30% inhibition of Na+ reabsorption when retroperfused at a concentration of 12.5 micrograms, as did kallikrein (176 micrograms) and trypsin (33.3 micrograms). These results indicate that prostaglandins and kinins can inhibit Na+ reabsorption in the rat parotid duct when present in the luminal side of the cells. Since they are normally present in exocrine glands and can presumably be secreted, they may have a role as luminal factors in the regulation of transductal transport of Na+. The possibility that they may be increased in the exocrine secretions of patients with cystic fibrosis and that they may act as the so-called cystic fibrosis "factors" is also raised by the findings of this study.