Drugs online research references
Pflugers Arch. 1987 Mar;408(3):275-81.
Electrodiffusion of Cl- and K+ in epithelial membranes reconstituted into planar lipid bilayers.
Zeuthen T, Christensen O, Cherksey B.
An electrodiffusive permeability for Cl-, its activation by low extracellular Cl--concentrations and the interaction between electrodiffusive fluxes of Cl- and K+ are demonstrated in the ventricular membranes from the epithelium of the bovine choroid plexus. Membranes were fused into artificial lipid bilayers formed at the tip of micropipettes. What is thought to be the cytoplasmic side of the membrane (the trans-side or the inside of pipette) was clamped at negative potentials (0 to -90 mV). Under these conditions the current was discrete, fluctuating less than 2 pA. With Cl- as the only conducting ion on the two sides we observed a small electrodiffusive permeability which was reduced by bumetanide or furosemide by 62%. When the outside solution was rendered Cl--free then the permeability to Cl- increased by a factor of 2-5; this activation was reduced by bumetanide or furosemide by about 80%. We observed an interaction between inwards movements of K+ and outwards movements of Cl- via the activated permeability: The total current was smaller than the sum of the expected inward K+-current and the expected outward activated Cl--current. Bumetanide or furosemide increased the total current; apparently the loss of current carried by Cl- was smaller than the gain in current carried by K+. The presence of K+ on both sides of the membrane was a condition for this interaction.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3575093&dopt=Abstract
J Membr Biol. 1986;92(2):135-50.
Kinetic mechanism of Na+, K+, Cl--cotransport as studied by Rb+ influx into HeLa cells: effects of extracellular monovalent ions.
Miyamoto H, Ikehara T, Yamaguchi H, Hosokawa K, Yonezu T, Masuya T.
Ouabain-insensitive, furosemide-sensitive Rb+ influx (JRb) into HeLa cells was examined as functions of the extracellular Rb+, Na+ and Cl- concentrations. Rate equations and kinetic parameters, including the apparent maximum JRb, the apparent values of Km for the three ions and the apparent Ki for K+, were derived. Results suggested that one unit molecule of this transport system has one Na+, one K+ and two Cl- sites with different affinities, one of the Cl- sites related with binding of Na+, and the other with binding of K+(Rb+). A 1:1 stoichiometry was demonstrated between ouabain-insensitive, furosemide-sensitive influxes of 22Na+ and Rb+, and a 1:2 stoichiometry between those of Rb+ and 36Cl-. The influx of either one of these ions was inhibited in the absence of any one of the other two ions. Monovalent anions such as nitrate, acetate, thiocyanate and lactate as substitutes for Cl- inhibited ouabain-insensitive Rb+ influx, whereas sulfamate and probably also gluconate did not inhibit JRb. From the present results, a general model and a specialized cotransport model were proposed: In HeLa cells, one Na+ and one Cl- bind concurrently to their sites and then one K+(Rb+) and another Cl- bind concurrently. After completion of ion bindings Na+, K+(Rb+) and Cl- in a ratio of 1:1:2 show synchronous transmembrane movements.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3761359&dopt=Abstract
Am J Physiol. 1987 Jan;252(1 Pt 2):F177-87.
ADH increases apical Na+, K+, 2Cl- entry in mouse medullary thick ascending limbs of Henle.
Molony DA, Reeves WB, Hebert SC, Andreoli TE.
These studies were designed to evaluate the mechanism for the ADH-dependent increase in transcellular conductance (Gc, mS X cm-2), which accompanies hormone-dependent increases in the spontaneous transepithelial voltage (Ve, mV) and in the net rate of Cl- absorption in single medullary thick ascending limbs of Henle (mTALH) isolated from mouse kidney. The total transepithelial conductance (Ge, mS X cm-2) was measured with perfusing solutions containing 5 mM K+, zero Ba2+; Gc was that component of Ge blocked by luminal 20 mM Ba2+, zero K+. In paired experiments, antidiuretic hormone (ADH) increased Gc from 44.5 +/- 5.6 to 58.9 +/- 8.9 mS X cm-2 (delta = 14.3 +/- 5.5; P less than 0.02); however, in the presence of 10(-4) M luminal furosemide, ADH had no significant effect on Gc (delta = 5.0 +/- 4.3; NS). A set of similarly paired measurements together with paired observations on the effects of bath Cl- deletion, permitted an assessment of the effect of ADH on the magnitude of the fall in Gc on bath Cl- removal (delta GClc, mS X cm-2). delta GClc was clearly larger with ADH, 29.6 +/- 4.3, than without ADH, 19.2 +/- 1.0 (delta = 10.4 +/- 4.9; P less than 0.05). However, with luminal furosemide, ADH had no significant effect on delta GClc (delta = 1.7 +/- 4.5; NS). These results indicate that the ADH-dependent increase in Gc is secondary to increased salt entry across the apical membrane. We computed apical (ga, mS X cm-2) and basolateral (gb, mS X cm-2) membrane conductances from the Gc measurements and apical-to-basolateral membrane resistance ratios (Ra/Rb) obtained from cell impalement: the ADH-dependent Gc increase was due to an increase in gb, which was blocked entirely by luminal furosemide. We propose that ADH increases the number of functioning apical membrane Na+,K+,2Cl- transport units, and that gb increases because cell Cl- activity rises and depolarizes the basolateral membrane. Thus the calculated cellular Cl- activity was 16.3 mM without ADH, and 25 mM with ADH.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3812700&dopt=Abstract
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