A discussion of Ambystoma kidney tubule ion channels, transporters, and pH regulation.

This paper explores the role and biophysical expression of the equivalent electrical circuit model as it applies to ionic conductances across the paracellular shunt, apical membrane, and basolateral membrane of the Ambystoma renal proximal tubule. Information about such conductances may be experimentally determined through transepithelial voltage and intracellular voltage measurements. The equivalent electrical circuit model has been applied extensively by investigators to define ion channels and transport mechanisms in the salamander proximal tubule. A comprehensive discussion of all known ionic conductance and transport pathways as well as pH-regulatory functions of contributory symports/antiports is examined in the Ambystoma proximal tubule. This paper explores renal physiological principles and serves as a companion to: Bock JF, Boulpaep EL: Bicarbonate transport mechanisms in the Ambystoma kidney proximal tubule: Transepithelial potential measurements.

Bicarbonate transport mechanisms in the Ambystoma kidney proximal tubule: transepithelial potential measurements.

Modes of bicarbonate entry from tubule lumen to cell were examined in isolated Ambystoma proximal tubules, using determinations of transepithelial potential differences (V3). (1) Upon removal of luminal substrate, tubules first equilibrated in bilateral (lumen and bath) 94.72 mM Cl- and 10 mM HCO3- yielded a change in V3 between the experimental and control circumstances of +1.8 mV (delta V3). (2) The identical experiment conducted under the condition of symmetrical 4.72 mM Cl- produced a delta V3 of +7.6 mV. This reduction of luminal and bath Cl- generates an amplification of delta V3 by a factor of 4.4 and reflects a substantial increase in the paracellular Cl- shunt resistance. Ensuing experiments were conducted in bilateral nominally Cl(-)-free solutions and in the absence of luminal substrate. The experimental protocols are divided into several situations where HCO3- is removed from the lumen, bath, or lumen and bath; the HCO3- removal sequences are repeated in the presence of luminal SITS and then after SITS washout. 0.5 mM SITS (4-acetoamido-4-isothiocyanostilbene-2,2'-disulfonate) was applied exclusively to the luminal perfusate. (1) Removal of luminal HCO3- in the absence of SITS produces a delta V3 of -1.9 mV, whereas, in the presence of SITS, the delta V3 measures -1.3 mV. Subsequent removal of luminal HCO3- in the presence of bath HCO3- (in the presence of luminal SITS) yields a delta V3 of -1.0 mV. All of these measurements reflect a decrease in HCO3- current across the basolateral membrane Na+ (HCO3-)n co-transporter; the role of a possible Cl-/Anion- antiport cannot be assessed. (2) Removal of bath HCO3- in the absence of SITS yields a delta V3 of +1.5 mV, whereas, in the presence of SITS, the delta V3 value measures +1.2 mV. Subsequent removal of bath HCO3- in the absence of luminal HCO3- (in the presence of SITS) yields a delta V3 of +0.8 mV. These experiments are consistent with an increase in HCO3- current across the basolateral Na+(HCO3-)n co-transporter, do not rule out the possibility of an apical HCO3- conductance pathway, and diminish the likelihood of an apical Cl-/HCO3- antiport system.

Liver cell adenoma: diagnosis and treatment of a rare hepatic neoplastic process.

Liver adenomatosis is a rare entity in which multiple liver cell adenomas (more than 10) occur in patients with no prior history of steroid use or glycogen storage disease. This report describes a case of liver adenomatosis, distinguishes liver adenomatosis from other benign liver lesions, and discusses the diagnosis and treatment of this disorder.