Total contents and net movements of magnesium in the rat uterus

1971 ◽  
Vol 220 (6) ◽  
pp. 2067-2067
Author(s):  
A. H. Moawad ◽  
E. E. Daniel

Page 75: A. H. Moawad and E. E. Daniel. "Total contents and net movements of magnesium in the rat uterus." Page 80, column 2, line 44, involving the calculation of Vm the answer to the equation, –0.067 V, should read, "–0.012 V." Page 80, column 2, lines 49–54 should read, "The calculated magnesium equilibrum potential is less than the observed membrane potential, which is about 0.050 V. Therefore, some of the tissue magnesium may be excluded by an active transport process against an electrochemical gradient or by loose binding in the extracellular space."

1986 ◽  
Vol 238 (2) ◽  
pp. 443-449 ◽  
Author(s):  
E F LaBelle ◽  
S V Singh ◽  
S K Srivastava ◽  
Y C Awasthi

Dinitrophenyl S-glutathione is accumulated by inside-out vesicles made from human erythrocytes in a process totally dependent on ATP and Mg2+. The vesicles were shown to accumulate dinitrophenyl S-glutathione against a concentration gradient. The vesicles were able to concentrate this glutathione derivative even in the absence of membrane potential. This indicated that the ATP-dependent uptake of dinitrophenyl S-glutathione by inside-out vesicles represented an active transport process. Neither extravesicular EGTA nor intravesicular ouabain inhibited the transport process, indicating that neither the Ca2+-ATPase nor the Na+, K+-ATPase were involved. These results indicated that dinitrophenyl S-glutathione uptake by inside-out vesicles probably represented primary active transport. The uptake of dinitrophenyl S-glutathione was a linear function of time (up to 5 h) and vesicle protein. The rate of uptake was optimal between pH 7.0 and 8.0 and at 37 degrees C. The Km values determined for dinitrophenyl S-glutathione and ATP were 0.29 mM and 1 mM, respectively. The transport process was completely inhibited by vanadate and by p-hydroxymercuribenzene sulphonate and inhibited to a lesser extent by N-ethylmaleimide. GTP could efficiently substitute for ATP as an energy source for the transport process, but CTP and UTP were comparatively much less effective.


1999 ◽  
Vol 112 (12) ◽  
pp. 2033-2041
Author(s):  
J.J. Ludtke ◽  
G. Zhang ◽  
M.G. Sebestyen ◽  
J.A. Wolff

Although the entry of DNA into the nucleus is a crucial step of non-viral gene delivery, fundamental features of this transport process have remained unexplored. This study analyzed the effect of linear double stranded DNA size on its passive diffusion, its active transport and its NLS-assisted transport. The size limit for passive diffusion was found to be between 200 and 310 bp. DNA of 310–1500 bp entered the nuclei of digitonin treated cells in the absence of cytosolic extract by an active transport process. Both the size limit and the intensity of DNA nuclear transport could be increased by the attachment of strong nuclear localization signals. Conjugation of a 900 bp expression cassette to nuclear localization signals increased both its nuclear entry and expression in microinjected, living cells.


1987 ◽  
Vol 252 (1) ◽  
pp. G100-G108
Author(s):  
J. H. Sellin ◽  
R. De Soignie

Active Na absorption (JNanet) in rabbit proximal colon in vitro is paradoxically stimulated as [Na] in the bathing media is lowered with constant osmolarity. At 140 mM [Na]o, JNanet is -0.6 +/- 0.4 mueq X cm-2 X h-1, whereas at 50 mM [Na]o JNanet is 5.0 +/- 0.7 mueq X cm-2 X h-1, P less than 0.01. JNas----m is a linear function of [Na]o, suggesting a diffusional flux. JNam----s increases almost linearly from 0 to 50 mM [Na]o but then plateaus and actually decreases from 50 to 140 mM [Na]o, consistent with inhibition of an active transport process. Both lithium and Na are equally effective inhibitors of JNanet, whereas choline and mannitol do not block the high rate of JNanet observed in decreased [Na]o. Either gluconate or proprionate replacement of Cl inhibits JNanet. Removal of K or HCO3 does not alter Na absorption. JNanet at lowered [Na]o is electrically silent and is accompanied by increased Cl absorption; it is inhibited by 10(-3) M amiloride and 10(-3) M theophylline but not by 10(-4) M bumetanide. Epinephrine is equally effective at stimulating Na absorption at 50 and 140 mM [Na]; yohimbine does not inhibit JNanet at 50 mM [Na]o. Na gradient experiments are consistent with a predominantly serosal effect of the decreased [Na]o. These results suggest that Na absorption in rabbit proximal colon in vitro is stimulated by decreased [Na]; the effect is cation specific, both Na and Li blocking the stimulatory effect.(ABSTRACT TRUNCATED AT 250 WORDS)


1966 ◽  
Vol 49 (3) ◽  
pp. 551-563 ◽  
Author(s):  
Ronald J. Poole

Intracellular potentials were measured in beetroot tissue during the steady-state uptake of K+ from various solutions. In solutions containing bicarbonate, the membrane potential becomes up to 70 mv more negative than the estimated equilibrium potential for K+. The uptake of K+ from such solutions is correlated with variations in the potential, both when the bicarbonate concentration is changed and also when the metabolic activity of the tissue is changed by washing in water for various periods. However, the estimated permeability to K+ varies from 0.4 x 10-7 to 1.5 x 10-7 cm·sec-1. It is postulated that the change of potential arises from the metabolic transport of HCO3- into the cell or H+ outwards, and that the associated uptake of K+ is partly or entirely by passive diffusion across the cell membrane. In contrast, K+ uptake from KCl solutions is not accompanied by any significant change in the membrane potential, which remains relatively close to the K+ equilibrium potential. In solutions containing both KHCO3 and KCl, it appears that an amount of K+ equal to the influx of Cl- is taken up independently of the potential, while the component of K+ uptake which is not balanced by Cl- uptake is related to the potential in the manner described. These results suggest that K+ uptake is linked to Cl- uptake in an electrically neutral active transport process.


1960 ◽  
Vol 198 (3) ◽  
pp. 609-613 ◽  
Author(s):  
Eugene B. Dowdle ◽  
David Schachter ◽  
Harris Schenker

Everted gut sacs prepared from segments of the proximal small intestine of rats transport Fe59 from the mucosal to the serosal surfaces against concentration gradients in vitro. The active transport mechanism is dependent upon oxidative metabolism and the generation of phosphate-bond energy, and is limited in capacity. The active transport process is maximal in the region of the small intestine immediately distal to the pylorus and diminishes with more distal segments of the gut. Addition of ascorbic acid to the incubation medium markedly increases the active transport of Fe59 in vitro.


2006 ◽  
Vol 21 (8) ◽  
pp. 2058-2067 ◽  
Author(s):  
Luke Matthews ◽  
Vishnu Baba Sundaresan ◽  
Victor Giurgiutiu ◽  
Donald J. Leo

Nastic structures are synthetic constructs capable of controllable deformation and shape change similar to plant motility, designed to imitate the biological process of nastic movement found in plants. This paper considers the mechanics and bioenergetics of a prototype nastic structure system consisting of an array of cylindrical microhydraulic actuators embedded in a polymeric plate. Non-uniform expansion/contraction of the actuators in the array may yield an overall shape change resulting in structural morphing. Actuator expansion/contraction is achieved through pressure changes produced by active transport across a bilayer membrane. The active transport process relies on ion-channel proteins that pump sucrose and water molecules across a plasma membrane against the pressure gradient. The energy required by this process is supplied by the hydrolysis of adenosine triphosphate. After reviewing the biochemistry and bioenergetics of the active transport process, the paper presents an analysis of the microhydraulic actuator mechanics predicting the resulting displacement and output energy. Experimental demonstration of fluid transport through a protein transporter follows this discussion. The bilayer membrane is formed from 1-Palmitoyl-2-Oleoyl-sn-Glycero-3-[Phospho-L-Serine] (Sodium Salt), 1-Palmitoyl-2-Oleoyl-sn-Glycero- 3-Phosphoethanolamine lipids to support the AtSUT4 H+-sucrose cotransporter.


1972 ◽  
Vol 60 (5) ◽  
pp. 519-533 ◽  
Author(s):  
J. M. Russell ◽  
A. M. Brown

We measured the internal potassium activity, aiK, and membrane potential, Em, simultaneously in 111 R2 giant neurons of Aplysia californica. aiK was 165.3 ± 3.4 mM, Em was -47.8 ± 0.9 mv, and EK calculated using the Nernst equation was -76.9 ± 0.05 mv. Such values were maintained for as long as 6 hr of continuous recording in untreated cells, aiK fell exponentially after the following treatments: cooling to 0.5°–4°C, ouabain, zero external potassium, 2,4-dinitrophenol, and cyanide. The effects of cooling and zero potassium were reversible. Potassium permeability was calculated from net potassium flux using the constant field equation and ranged from 2.6 to 18.5 x 10-8 cm/sec. We conclude that potassium is actively transported into this neuron against a 30–40 mv electrochemical gradient.


1954 ◽  
Vol 1 (1) ◽  
pp. 36-44 ◽  
Author(s):  
Anna Maria Williams ◽  
P. W. Wilson

Sucrose-grown (unadapted) and succinate-grown (adapted) cells were mixed with various concentrations of succinate at 3 °C. under air and at 30 °C. under helium. The amount of succinate removed from the external solution by the cells was proportional to the concentration of succinate and did not differ significantly with the two types of cells. Although the data did not differentiate between equilibration with intracellular water and mere adsorption, they indicate that no change has occurred in the surface of the adapted cells to allow a more rapid diffusion of succinate across the osmotic barrier under nonmetabolic conditions. So far as can be determined by using masses of cells, any "permeability" changes during adaptation of the azotobacter cells to succinate must be connected with an active transport process associated with metabolism.


1965 ◽  
Vol 43 (4) ◽  
pp. 551-577 ◽  
Author(s):  
E. E. Daniel

The mechanisms underlying the periodic depolarizations (slow waves) in longitudinal muscle of the small intestine were studied in vivo in dogs by means of intra-arterial perfusions of solutions with altered electrolyte concentrations or with added metabolic inhibitors. Perfusion of solutions containing reduced sodium, potassium, or chloride concentrations markedly altered electrolyte concentrations in intestinal muscle but did not necessarily alter intestinal slow waves seriously. However, when lithium ion was substituted for sodium ion serious depression of slow waves occurred. This was also found with ouabain, NaF, and Na2EDTA, substances which, like lithium, are believed to inhibit the active transport process directly. Iodoacetate and dinitrophenol had little depressant effect on intestinal slow waves in amounts sufficient to cause downhill ion movements. NaCN or 1,10-phenanthroline depressed slow waves, but the effect of NaCN was largely prevented by prior reserpinization of the dog. The depressant effects of lithium ion, ouabain, NaF, and Na2EDTA were diminished but not abolished by reserpinization. It was concluded that lower amounts of inhibitors of the active transport process abolished intestinal slow waves by causing the release of catecholamines from intrinsic nerve endings in the intestine. The released catecholamines then depressed slow waves. In higher amounts, inhibitors of the active transport process depressed intestinal slow waves by a direct action, unaffected by reserpinization. Intestinal slow waves were therefore postulated to originate from the oscillatory activity of an electrogenic sodium pump.Perfusates with elevated sodium or potassium concentration initiated action potentials in intestinal longitudinal muscle. These action potentials were blocked by atropine and hexamethonium. In reserpinized animals, Na2EDTA or large amounts of ouabain also initiated action potentials which were stopped or prevented by atropine. It was postulated that all these procedures caused acetylcholine release from intrinsic parasympathetic nerves and that the common mechanism was displacement of mediator by net entrance of sodium ion. This same mechanism may also have accounted for the release of catecholamines from intrinsic sympathetic nerves mentioned above.


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