Intracellular potassium activity and the role of potassium in transepithelial salt transport in the human reabsorptive sweat duct

1991 ◽  
Vol 119 (3) ◽  
pp. 199-210 ◽  
Author(s):  
M. M. Reddy ◽  
P. M. Quinton
Keyword(s):  
Salt Transport ◽  
Sweat Duct ◽  
Intracellular Potassium ◽  
Intracellular Potassium Activity

Role of thyroxine on postnatal development of ileal active bile salt transport

1986 ◽  
Vol 251 (2) ◽  
pp. G237-G242 ◽  
Author(s):  
J. E. Heubi
Keyword(s):  
Thyroid Hormone ◽  
Postnatal Development ◽  
Active Transport ◽  
Salt Transport ◽  
Maximal Velocity ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Taurocholate Transport

The role of thyroid hormone on the postnatal development of ileal active taurocholate transport uptake was measured by an in vitro incubation technique in Sprague-Dawley rats. In 16-day-old rats treated with pharmacological doses of L-thyroxine (50 micrograms X 100 g body wt-1 X day-1 on days 10-13), ileal active transport appeared precociously whose Km was 1.60 +/- 0.48 mM and Vapp (apparent maximal velocity) was 8.09 +/- 1.14 nmol X min-1 X mg dry wt-1, while age-matched shams had only passive diffusion of taurocholate. To determine whether enhanced endogenous secretion of thyroxine was capable of stimulating development of ileal active taurocholate transport, thyrotrophic stimulating hormone (TSH) (0.5 U/100 g body wt twice daily) was given on days 10-13, with uptake measured on day 16. Following TSH treatment, only passive transport for taurocholate was observed in the ileum; uptake rates were consistently higher than those for untreated controls at each study concentration. Thyroidectomy performed at age 14 days with uptake measured at age 21 days did not ablate development of ileal active transport but resulted in a significant reduction (P less than 0.001) in the Vapp (7.39 +/- 1.10 nmol X min-1 X mg dry wt-1) and a significant increase (P less than 0.014) in Km (1.72 +/- 0.53 mM) compared with age-matched controls. Thyroid hormone does not appear to be obligatory for the postnatal development of ileal active taurocholate transport.

Intracellular potassium activities in Amphiuma small intestine

1976 ◽  
Vol 231 (4) ◽  
pp. 1214-1219 ◽  
Author(s):  
JF White
Keyword(s):  
Small Intestine ◽  
Membrane Potential ◽  
Activity Coefficient ◽  
Potassium Concentration ◽  
Equilibrium Potential ◽  
Absorptive Cell ◽  
Buffer Solution ◽  
Intracellular Potassium ◽  
Intracellular Potassium Activity ◽  
Liquid Ion Exchanger

Intracellular potassium activity (aKi) has been determined in absorptive cells lining the villi of isolated, stripped proximal segments of Amphiuma small intestine. With single-barreled liquid ion-exchanger microelectrodes aKi = 41.6 +/- 1.5 mM in normal chloride buffer; with double-barreled microelectrodes constructed by a new method aKi = 38.5 +/- 2.4 mM. Also, by the latter approach aKi = 41.1 +/- 2.1 mM in buffer in which potassium was elevated to 5 meq/liter and aKi = 44.2 +/- 1.3 mM in sulfate buffer with the same bath potassium concentration. Since the calculated potassium equilibrium potential exceeds the membrane potential this ion is accumulated by the intestinal absorptive cell. A major portion of cellular potassium is bound or compartmentalized since the intracellular potassium activity coefficient is very low. A layer exists near the villi in which the potassium activity exceeds that in the bath buffer solution.

scholarly journals Role of Time Relaxation in a One-Dimensional Diffusion-Advection Model of Water and Salt Transport

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Igor Medved’ ◽  
Robert Černý
Keyword(s):  
Diffusion Coefficient ◽  
Structural Damage ◽  
Building Materials ◽  
Chloride Transport ◽  
Salt Transport ◽  
One Dimensional ◽  
Advection Diffusion ◽  
Dimensional Diffusion ◽  
Lime Plaster

The transport of salt, necessarily coupled with the transport of water, through porous building materials may heavily limit their durability due to possible deterioration and structural damage. Usually, the binding of salt to the pore walls is assumed to occur instantly, as soon as the salt is transported by water to a given position. We consider the advection-diffusion model of the transport and generalize it to include possible delays in the binding. Applying the Boltzmann-Matano method, we calculate the diffusion coefficient of the salt in dependence on the salt concentration and show that it increases with the rate of binding. We apply our results to an example of the chloride transport in a lime plaster.

Preserved macula densa-dependent renin secretion in A1 adenosine receptor knockout mice

2003 ◽  
Vol 284 (4) ◽  
pp. F770-F777 ◽  
Author(s):  
Frank Schweda ◽  
Charlotte Wagner ◽  
Bernhard K. Krämer ◽  
Jürgen Schnermann ◽  
Armin Kurtz
Keyword(s):  
Mrna Expression ◽  
Glomerular Filtration ◽  
Knockout Mice ◽  
Macula Densa ◽  
Salt Transport ◽  
Renin Secretion ◽  
Renin Mrna ◽  
Renin Content

Recent studies demonstrated that the influence of the macula densa on glomerular filtration is abolished in adenosine A1 receptor (A1AR) knockout mice. Inasmuch as the macula densa not only regulates glomerular filtration but also controls the activity of the renin system, the present study aimed to determine the role of the A1AR in macula densa control of renin synthesis and secretion. Although a high-salt diet over 1 wk suppressed renin mRNA expression and renal renin content to similar degrees in A1AR+/+, A1AR+/−, and A1AR−/−mice, stimulation of Ren-1 mRNA expression and renal renin content by salt restriction was markedly enhanced in A1AR−/− compared with wild-type mice. Pharmacological blockade of macula densa salt transport with loop diuretics stimulated renin expression in vivo (treatment with furosemide at 1.2 mg/day for 6 days) and renin secretion in isolated perfused mouse kidneys (treatment with 100 μM bumetanide) in all three genotypes to the same extent. Taken together, our data are consistent with the concept of a tonic inhibitory role of the A1AR in the renin system, whereas they indicate that the A1AR is not indispensable in macula densa control of the renin system.

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