Lohrmann E, Burhoff I, Nitschke R B, Lang H J, Mania D, Englert H C, Hropot M, Warth R, Rohm W, Bleich M
Physiologisches Institut der Albert-Ludwigs-Universität, Freiburg, Germany.
Pflugers Arch. 1995 Feb;429(4):517-30. doi: 10.1007/BF00704157.
Previously we have shown that arylaminobenzoates like 5-nitro-2-(3-phenylpropylamino)-benzoate (NPPB), which are very potent inhibitors of NaCl absorption in the thick ascending limb of the loop of Henle, are only poor inhibitors of the cAMP-mediated secretion of NaCl in rat colon. This has prompted our search for more potent inhibitors of NaCl secretion in the latter system. The chromanole compound 293 B inhibited the equivalent short-circuit current (Isc) induced by prostaglandin E2 (n = 7), vasoactive intestinal polypeptide (VIP, n = 5), adenosine (n = 3), cholera toxin (n = 4) and cAMP (n = 6), but not by ionomycin (n = 5) in distal rabbit colon half maximally (IC50) at 2 mumol/l from the mucosal and at 0.7 mumol/l from the serosal side. The inhibition was reversible and paralleled by a significant increase in transepithelial membrane resistance [e.g. in the VIP series from 116 +/- 16 omega.cm2 to 136 +/- 21 omega.cm2 (n = 5)]. A total of 25 derivatives of 293 B were examined and structure activity relations were obtained. It was shown that the racemate 293 B was the most potent compound within this group and that its effect was due to the enantiomer 434 B which acted half maximally at 0.25 mumol/l. Further studies in isolated in vitro perfused colonic crypts revealed that 10 mumol/l 293 B had no effect on the membrane voltage across the basolateral membrane (Vbl) in non-stimulated crypt cells: -69 +/- 3 mV versus -67 +/- 3 mV (n = 10), whilst in the same cells 1 mmol/l Ba2+ depolarised Vbl significantly. However, 293 B depolarised Vbl significantly in the presence of 1 mumol/l forskolin: -45 +/- 4 mV versus -39 +/- 5 mV (n = 7). Similar results were obtained with 0.1 mmol/l adenosine. 293 B depolarised Vbl from -40 +/- 5 mV to -30 +/- 4 mV (n = 19). This was paralleled by an increase in the fractional resistance of the basolateral membrane. VIP had a comparable effect. The hyperpolarisation induced by 0.1 mmol ATP was not influenced by 10 mumol/l 293 B: -75 +/- 6 mV versus -75 +/- 6 mV (n = 6). Also 293 B had no effect on basal K+ conductance (n = 4). Hence, we conclude that 293 B inhibits the K+ conductance induced by cAMP. This conductance is apparently relevant for Cl- secretion and the basal K+ conductance is insufficient to support secretion.
此前我们已经表明,像5-硝基-2-(3-苯基丙基氨基)苯甲酸酯(NPPB)这样的芳氨基苯甲酸酯,是亨利氏袢升支粗段中NaCl重吸收的强效抑制剂,但对大鼠结肠中cAMP介导的NaCl分泌的抑制作用却很弱。这促使我们去寻找后一系统中更有效的NaCl分泌抑制剂。色满醇化合物293 B抑制了前列腺素E2(n = 7)、血管活性肠肽(VIP,n = 5)、腺苷(n = 3)、霍乱毒素(n = 4)和cAMP(n = 6)在兔远端结肠诱导的等效短路电流(Isc),但对离子霉素(n = 5)诱导的电流无抑制作用,其半数最大抑制浓度(IC50)在黏膜侧为2 μmol/l,浆膜侧为0.7 μmol/l。这种抑制是可逆的,同时跨上皮膜电阻显著增加[例如在VIP组中,从116±16 Ω·cm²增加到136±21 Ω·cm²(n = 5)]。共检测了293 B的25种衍生物,并得出了构效关系。结果表明,外消旋体293 B是该组中最有效的化合物,其作用归因于对映体434 B,后者的半数最大作用浓度为0.25 μmol/l。在离体灌注结肠隐窝的进一步研究中发现,10 μmol/l 293 B对未受刺激的隐窝细胞基底外侧膜(Vbl)的膜电压无影响:分别为-69±3 mV和-67±3 mV(n = 10),而在相同细胞中,1 mmol/l Ba²⁺可使Vbl显著去极化。然而,在存在1 μmol/l福斯高林的情况下,293 B可使Vbl显著去极化:分别为-45±4 mV和-39±5 mV(n = 7)。用0.1 mmol/l腺苷也得到了类似结果。293 B使Vbl从-40±5 mV去极化至-30±4 mV(n = 19)。同时基底外侧膜的电阻分数增加。VIP有类似作用。0.1 mmol ATP诱导的超极化不受10 μmol/l 293 B影响:分别为-75±6 mV和-75±6 mV(n = 6)。293 B对基础K⁺电导也无影响(n = 4)。因此,我们得出结论,293 B抑制cAMP诱导的K⁺电导。这种电导显然与Cl⁻分泌有关,而基础K⁺电导不足以支持分泌。