Ionic basis of membrane potentials of epithelial cells in rat small intestine

Barry, R. J. C.; Eggenton, Jacqueline

doi:10.1113/jphysiol.1972.sp010028

Cited by 17 publications

(7 citation statements)

References 14 publications

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“…Origin of the microvillar membrane potential (Vm) The microvillar membrane potential of mammalian small intestine, measured in the absence of actively transported non-electrolyte, depends on Na+ and K+ (McKenney, 1969;Rose & Schultz, 1971;Ellory et al 1972;Barry & Eggenton, 1972;Okada et al 1975;van Os & Slegers, 1975;Reuss & Finn, 1975), but not on Cl- (Rose & Schultz, 1971;Barry & Eggenton, 1972;Okada et al 1975). Vm for the large intestine shows a Cl-dependence, the effect of other monovalent ions being more debatable.…”

Section: Discussionmentioning

confidence: 99%

Electrical properties of pig colonic mucosa measured during early post‐natal development.

Hénin¹,

Smith²

1976

The Journal of Physiology

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SUMMARY1. Microvillar membrane (Vm) and transmural (Vt) potential differences were measured in proximal colon taken from pigs at birth and up to 10 days of age.2. Vm remained independent of the age of the animal provided it was measured in the absence of methionine. The over-all mean was -43-3 mV. Adding methionine to fluid bathing the mucosal surface of new-born pig colon caused a 9-8 mV depolarization of Vm and a 6-7 mV increase in Vt. These effects, which were Na+-dependent, were not seen in the 10-day-old animal.3. Substituting S042-for Cl-in methionine-free medium caused a hyperpolarization in Vm. Increasing the concentration of K+ caused corresponding depolarization. Substituting choline for Na+ had no effect on Vm. Cl-and K+ movement across the microvillar membrane together account for the bulk of the measured membrane potential. These results apply to all stages of development.4. Na+ uptake across the microvillar membrane of the new-born pig colon was increased in the presence of methionine. This effect disappeared in older animals. Na+ uptake in the absence of methionine doubled during the first 24 h of post-natal life. This increase was maintained using colons taken from older animals.5. Methionine depolarization of Vm in the new-born pig colon is probably caused by the electrogenic influx of Na+. The ability of the colon to actively concentrate methionine within its mucosa disappears at the same time as methionine ceases to affect Vm and Vt. It is suggested that methionine and Na+ form a ternary complex with a carrier in the brush border of the new-born pig colon and that this carrier is lost or modified during early post-natal development.

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Section: Discussionmentioning

confidence: 99%

Electrical properties of pig colonic mucosa measured during early post‐natal development.

Hénin¹,

Smith²

1976

The Journal of Physiology

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“…This information is now crucial to our understanding of the relationship between Na+ and K+ diffusion potentials and measured values of Vm. The changes in Vm observed are unlikely to be due to alterations in Cl-concentration in the mucosal fluid since it has been shown that Cl-makes no apparent contribution to Vm in either fed or fasted animals (Rose & Schultz, 1971;Barry & Eggenton, 1972;Okada et al 1975).…”

Section: Effects Of Sugars and Amino Acidsmentioning

confidence: 99%

The effect of fasting on the potential difference across the brush‐border membrane of enterocytes in rat small intestine.

Debnam¹,

Thompson²

1984

The Journal of Physiology

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SUMMARY1. The effects of starvation on the magnitude of the potential difference across the brush-border membrane of rat small intestine (Vm) have been studied in vitro.2. The mean values obtained for Vm in jejunal tissue after a fast of either 24 or 72 h duration (-53-5 and -55-0 mV respectively) were significantly greater than the mean value of -45-3 mV recorded using intestine from fed rats. A similar hyperpolarization was observed after a 72 h fast using intestine from a more distal region. The response to fasting seen in the jejunum appears to be caused by a decrease in Na+ permeability of the mucosal membrane.3. The addition ofD-galactose (4 mM) or L-valine (4 mM) to the mucosal fluid caused a depolarization of Vm. Using jejunum from fed animals, Vm in the presence of galactose and valine was found to be -403 and -39-2 mV respectively. Following a fast of 72 h duration, the values of Vm for the two substrates were -43-4 and -43-1 mV respectively. Phlorhizin (10-4 M) abolished the galactose-induced depolarization in both fed and fasted conditions but was without effect on the response to valine.4. It is concluded that starvation increases the electrical driving force for Na+ during Na+-coupled non-electrolyte transport into the enterocyte. The possible mechanisms involved in this adaptive response are discussed.

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“…The coefficients were then adjusted by trial and error until reasonable re-sponses were observed, primarily in the membrane potential. The most prominent adjustments were made in the apical permeability for K ϩ (P K a ), which was reduced to be in the same order of magnitude as the apical permeability for Na ϩ (P Na a ) as reported for rat small intestine (4), and the basolateral Na ϩ permeability (P Na bl ), which was increased since it in Ref. 1 was set to zero.…”

Section: Integrative Modelmentioning

confidence: 99%

“…However, some adjustments of the ionic permeabilities had to be done as we found little usable data on permeability coefficients for enterocytes. Studies exists (4,17), but they are old and unreliable. Measurements are typically done for whole tissue layers without blocking nondiffusive pathways for active transport and cotransport.…”

Section: Integrative Modelmentioning

confidence: 99%

Transepithelial glucose transport and Na⁺/K⁺ homeostasis in enterocytes: an integrative model

Thorsen

Drengstig

Ruoff

2014

American Journal of Physiology-Cell Physiology

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Thorsen K, Drengstig T, Ruoff P. Transepithelial glucose transport and Na ϩ /K ϩ homeostasis in enterocytes: an integrative model. Am J Physiol Cell Physiol 307: C320 -C337, 2014. First published June 4, 2014; doi:10.1152/ajpcell.00068.2013.-The uptake of glucose and the nutrient coupled transcellular sodium traffic across epithelial cells in the small intestine has been an ongoing topic in physiological research for over half a century. Driving the uptake of nutrients like glucose, enterocytes must have regulatory mechanisms that respond to the considerable changes in the inflow of sodium during absorption. The Na-K-ATPase membrane protein plays a major role in this regulation. We propose the hypothesis that the amount of active Na-K-ATPase in enterocytes is directly regulated by the concentration of intracellular Na ϩ and that this regulation together with a regulation of basolateral K permeability by intracellular ATP gives the enterocyte the ability to maintain ionic Na ϩ /K ϩ homeostasis. To explore these regulatory mechanisms, we present a mathematical model of the sodium coupled uptake of glucose in epithelial enterocytes. Our model integrates knowledge about individual transporter proteins including apical SGLT1, basolateral Na-K-ATPase, and GLUT2, together with diffusion and membrane potentials. The intracellular concentrations of glucose, sodium, potassium, and chloride are modeled by nonlinear differential equations, and molecular flows are calculated based on experimental kinetic data from the literature, including substrate saturation, product inhibition, and modulation by membrane potential. Simulation results of the model without the addition of regulatory mechanisms fit well with published short-term observations, including cell depolarization and increased concentration of intracellular glucose and sodium during increased concentration of luminal glucose/sodium. Adding regulatory mechanisms for regulation of Na-K-ATPase and K permeability to the model show that our hypothesis predicts observed long-term ionic homeostasis.enterocytes; epithelial transport; homeostasis; mathematical modeling; ionic regulation THE UPTAKE AND TRANSPORT OF glucose by the epithelial enterocytes in the small intestine are essential steps in all higher animals. Much of the glucose uptake in the small intestine is coupled to transport of sodium, and the different transporter proteins involved in the sodium coupled glucose uptake are well known (23,61,67,97). Although the electrochemical kinetics of the individual transporter proteins responsible for glucose and nutrient uptake are fairly elucidated (19,54,67,82,97), the combined function in which these transporters drive a net inflow of nutrients from the intestinal lumen to the serosal blood has not yet been modeled in detail.We have developed a mathematical model of an enterocyte that incorporates the available kinetic data from studies on individual transporter proteins. The model includes apical SGLT1 (the glucose sodium cotransporter), coupled apical flow of Na ϩ an...

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Ionic basis of membrane potentials of epithelial cells in rat small intestine

Cited by 17 publications

References 14 publications

Electrical properties of pig colonic mucosa measured during early post‐natal development.

Electrical properties of pig colonic mucosa measured during early post‐natal development.

The effect of fasting on the potential difference across the brush‐border membrane of enterocytes in rat small intestine.

Transepithelial glucose transport and Na⁺/K⁺ homeostasis in enterocytes: an integrative model

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Ionic basis of membrane potentials of epithelial cells in rat small intestine

Cited by 17 publications

References 14 publications

Electrical properties of pig colonic mucosa measured during early post‐natal development.

Electrical properties of pig colonic mucosa measured during early post‐natal development.

The effect of fasting on the potential difference across the brush‐border membrane of enterocytes in rat small intestine.

Transepithelial glucose transport and Na+/K+ homeostasis in enterocytes: an integrative model

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Transepithelial glucose transport and Na⁺/K⁺ homeostasis in enterocytes: an integrative model