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Biomedical subjects

M Peterlik

Publications and source records attributed to M Peterlik.

At least 109 records · Page 6Linked to original sources
PubMed1977

Effect of vitamin D3 and 1,25-dihydroxyvitamin D3 on intestinal transport of phosphate.

Dietary variations (low calcium, low calcium, low phosphorus, or high strontium) change phosphate transport by the jejunum according to their respective ability to increase or block the synthesis of 1,25-dihydroxyvitamin D3, suggesting that the action of this active sterol underlies the response of intestinal phosphate absorption to vitamin D. 1,25-(OH)2D3 stimulates the active entry of Pi at the mucosal border by its action on protein synthesis. It is attractive to speculate that 1,25-(OH)2D3 might induce the synthesis of a "phosphate carrier" protein in the plasma membrane. The interpretation that the enhancement of the maximal velocity of the "phosphate pump" by vitamin D is due to the creation of new pump sites would be consistent with this hypothesis.

Anaerobiosis↗
PubMed1976

Investigations on the sodium dependence of bile acid fluxes in the isolated perfused rat liver.

At [Na+]o = 118 mM the concentrative transfer of cholic and taurocholic acid from the perfusate into the isolated rat liver displays saturation kinetics (taurocholate: V = 299 nmol-min-1-g-1, Km = 61 muM; Cholate: V=327 nmol-min-1-g-1, Km = 436 muM). Perfusion with an isotonic sodium-free medium did not change the feature of a carrier-mediated transport but did markedly reduce V without affecting Km (taurocholate: V = 65 nmol-min-1-g-1, Km = 78 muM; cholate: V = 104 nmol-min-1-g-1, Km = 354 muM). It was experimentally assured that the observed reduction of bile salt uptake was not a consequence of regurgitation of bile salts or due to an excessive intracellular accumulation during cholestasis in the sodium-free state. The rate of taurocholate efflux is very low when compared with the rapid rate of the uptake. A stimulatory action of extracellular sodium on this pathway was also observed. Inhibition of the (Na+ + K+)-ATPase by 1 mM ouabain resulted in a decrease of bile salt uptake. Activation of the enzyme by potassium readmission to a K+-deprived liver enhanced bile salt uptake. The immediate response to alteration of the enzyme activity suggests a close association of a fraction of bile acid active transport with the sodium pump.

Adenosine Triphosphatases↗
PubMed1976

Ouabain-mediated sodium uptake and bile formation by isolated perfused rat liver.

Ouabain exhibits a dose-dependent choleretic effect in the isolated perfused rat liver. Its uptake from the perfusate into the liver is maintained against a concentration gradient and becomes clearly saturated at higher perfusate concentrations. A low extracellular sodium concentration inhibits the rate of ouabain transfer into liver cells, resulting in a marked decrease of the maximal transport rate. Dibucaine completely abolishes the uptake of the glycoside by the isolated liver. Determination of Na-22 tracer fluxes suggests that ouabain uptake is accompanied by a net flux of sodium into the cell, which seems to be due to a cotransport of sodium with ouabain rather than to the inhibition of the sinusoidal Na+ -K+ -ATPase. Sodium introduced into the cell in this way apparently is extruded into the bile canaliculi. The increase of isotonic bile flow, which is simultaneously observed, points to a dilution of the canalicular sodium gradient by water and electrolytes through an intercellular pathway. Our results present further evidence that bile secretion is controlled by transcellular sodium movements.

Anesthetics, Local↗