Carvounis C P, Carvounis G, Bernstein C, Oros M E
Department of Medicine, SUNY Health Science Center, Syracuse.
Biol Cell. 1989;66(1-2):43-51.
In agreement with previous reports, we found that absence of K+ from the serosal bath of the toad urinary bladder substantially impairs vasopressin and cAMP-stimulated water flow. The decreased response to vasopressin appears unrelated to prostaglandin production since inhibition of endogenous prostaglandins by pretreatment with naproxen 10(-5) M failed to prevent the effect seen with K+-free Ringer's. The resistance to vasopressin does not appear to be directly related to epithelial K+ concentrations, in that maneuvers leading to decreased intracellular K+ failed to produce a similar effect. A more likely explanation appears to be that K+-free Ringer's induces an increased cytosolic Ca++ which, in turn, decreases the hydrosmotic effects of vasopressin. Several lines of evidence argue in favor of such an explanation: (a) Increased cytosolic Ca++ had been found in other tissues with low extracellular K+; (b) The resistance to vasopressin decreases with decreased serosal Ca++; (c) The effects of K+-free Ringer's are not additive in situations believed to have increased epithelial Ca++, i.e. replacement of serosal Na+ with choline; (d) The effects of K+-free serosal bathing medium could be both prevented and/or reversed if already established by increasing serosal bath, and presumably intracellular, pH, which is believed to decrease intracellular Ca++.
与先前的报道一致，我们发现蟾蜍膀胱浆膜浴中缺乏钾离子会显著损害血管加压素和环磷酸腺苷刺激的水流量。对血管加压素反应的降低似乎与前列腺素的产生无关，因为用10(-5)M萘普生预处理抑制内源性前列腺素并不能阻止无钾林格氏液所产生的效应。对血管加压素的抵抗似乎与上皮细胞钾离子浓度没有直接关系，因为导致细胞内钾离子减少的操作未能产生类似的效应。一个更可能的解释似乎是无钾林格氏液会诱导细胞溶质钙离子增加，进而降低血管加压素的渗透作用。几条证据支持这样的解释：(a) 在细胞外钾离子浓度低的其他组织中已发现细胞溶质钙离子增加；(b) 对血管加压素的抵抗随着浆膜钙离子浓度降低而降低；(c) 在认为上皮细胞钙离子增加的情况下，即用胆碱替代浆膜钠离子时，无钾林格氏液的效应不会叠加；(d) 如果已经通过增加浆膜浴以及推测的细胞内pH值（据信会降低细胞内钙离子）来建立无钾浆膜浴介质的效应，那么其效应可以被预防和/或逆转。
