Murthy S N, Lavy A
Division of Gastroenterology, Hahnemann University, Philadelphia, PA 19102.
Biochem Pharmacol. 1988 Mar 15;37(6):1027-31. doi: 10.1016/0006-2952(88)90505-9.
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.
我们研究了二价阳离子钙（Ca2+）、单价阳离子钾（K+）和钠（Na+）以及影响这些阳离子通量的不同方式对犬十二指肠黏膜体外免疫反应性促胰液素（IRS）分泌的影响。在无细胞外Ca2+的情况下，基础IRS分泌受到29%的抑制。通过被动扩散增加Ca2+摄取以及通过离子载体A23187促进Ca2+摄取对基础IRS分泌无影响。然而，Ca2+通道阻滞剂LaCl3和维拉帕米分别使基础IRS分泌抑制了18%和33%。高浓度的细胞外K+引起IRS分泌呈剂量依赖性但延迟的刺激。K+刺激的IRS分泌不是由神经介导的。同样，阻断K+交换的9-氨基吖啶模拟了K+的作用。缬氨霉素（10(-6) M）抑制了K+刺激的和9-氨基吖啶刺激的IRS分泌。在无细胞外Na+的情况下，基础和K+刺激的IRS分泌均出现延迟抑制。这些结果表明阳离子环境的变化与IRS分泌的改变有关。高细胞外K+浓度有利于IRS分泌，而无细胞外Na+和Ca2+则对IRS分泌有抑制作用。
