Hirschowitz B I
Division of Gastroenterology, University of Alabama, Birmingham.
J Pharmacol Exp Ther. 1987 Nov;243(2):501-6.
To determine possible sites and mechanisms of action of somatostatin (SS) in gastric secretory mucosa, secretion of pepsin, H+, Cl-, Na+ and K+ was stimulated in conscious fistula dogs by i.v. infusion of bethanechol, pentagastrin and histamine in the absence and presence of SS-14. At low dose (0.5 micrograms or 300 pmol/kg/h), SS-14 potently inhibited H+ and pepsin stimulated by bethanechol (80 micrograms/kg/h) to less than 5% of control; it required 2 micrograms or 1200 pmol/kg/h of SS-14 to achieve similar inhibition of pentagastrin (1.5 micrograms/kg/h)-stimulated secretion. In both cases, gastric [K+] was depressed by SS-14 infusion and recovered before H+ and pepsin. Similar sensitivity to SS suggests a Ca++-dependent mechanism or pathway of stimulation by gastrin similar to that by cholinergic agonists. By contrast, histamine, which acts via cyclic AMP pathways, was not inhibited by a large dose of SS-14 (20 micrograms/kg/h). SS inhibition is thus agonist (or pathway)- rather than organ- or cell-specific.
为确定生长抑素（SS）在胃分泌性黏膜中的可能作用部位及机制，在有意识的瘘管犬中，于给予和不给予SS - 14的情况下，通过静脉输注氨甲酰甲胆碱、五肽胃泌素和组胺来刺激胃蛋白酶、H⁺、Cl⁻、Na⁺和K⁺的分泌。在低剂量（0.5微克或300皮摩尔/千克/小时）时，SS - 14能有效抑制由氨甲酰甲胆碱（80微克/千克/小时）刺激产生的H⁺和胃蛋白酶分泌，使其降至对照值的5%以下；而需要2微克或1200皮摩尔/千克/小时的SS - 14才能对五肽胃泌素（1.5微克/千克/小时）刺激的分泌产生类似的抑制作用。在这两种情况下，输注SS - 14会使胃内[K⁺]降低，且在H⁺和胃蛋白酶恢复之前就恢复了。对SS的类似敏感性表明，胃泌素刺激的钙依赖机制或途径与胆碱能激动剂刺激的类似。相比之下，通过环磷酸腺苷途径起作用的组胺，不会被大剂量的SS - 14（20微克/千克/小时）抑制。因此，SS的抑制作用是激动剂（或途径）特异性的，而非器官或细胞特异性的。
