Cationic environment and secretin secretion in canine duodenal mucosa in vitro.
We examined the effects of the divalent cation calcium (Ca2+) and the monovalent cations potassium (K+) and sodium (Na+) and different modalities that affect the fluxes of these cations on immunoreactive secretin (IRS) secretion from canine duodenal mucosa in vitro. In the absence of extracellular Ca2+, the basal IRS secretion was inhibited by 29%. Increased uptake of Ca2+ by passive diffusion and facilitated uptake of Ca2+ by ionophore A23187 had no effect on basal IRS secretion. However, Ca2+ channel blocking agents, LaCl3 and verapamil, inhibited basal IRS secretion by 18 and 33% respectively. High concentrations of extracellular K+ caused a dose-dependent but delayed stimulation of IRS secretion. K+-stimulated IRS secretion was not neurally mediated. Similarly, 9-aminoacridine, which blocks K+ exchange, mimicked the effects of K+. Valinomycin (10(-6) M) inhibited both K+-stimulated and 9-aminoacridine-stimulated IRS secretion. In the absence of extracellular Na+, there was a delayed inhibition of both basal and K+-stimulated IRS secretion. These results suggest that changes in cationic environment are associated with alterations in the secretion of IRS. High extracellular K+ concentration is conducive, and the absence of extracellular Na+ and Ca2+ is inhibitory to IRS secretion.
Murthy
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Division of Gastroenterology, Hahnemann University, Philadelphia, PA 19102.
Lavy
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A
D000585:Aminacrine / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000494:pharmacology*; D004285:Dogs; D004386:Duodenum / Q000378:metabolism; D005260:Female; D066298:In Vitro Techniques; D007413:Intestinal Mucosa / Q000378:metabolism; D011188:Potassium / Q000494:pharmacology*; D012633:Secretin / Q000378:metabolism*; D012964:Sodium / Q000494:pharmacology*; D014634:Valinomycin / Q000494:pharmacology
D012633:Secretin; D014634:Valinomycin; D000585:Aminacrine; D012964:Sodium; D011188:Potassium; D002118:Calcium