Drugs online research references
Lens Eye Toxic Res. 1990;7(2):103-19.
Effect of PO2 and metabolic inhibitors on ionic fluxes across the isolated rabbit corneal endothelium.
Green K, Cheeks L, Armstrong E, Berdecia R, Kramer K, Hull DS.
Department of Ophthalmology, Medical College of Georgia, Augusta 30912.
Bicarbonate and sodium fluxes were measured across the isolated rabbit corneal endothelium under the influence of several inhibitors. Depression of PO2 in the bathing medium decreased net sodium movement but increased bicarbonate movement. Furosemide did not alter bicarbonate fluxes at either 10(-4) or 10(-5) M, but increased passive sodium flux leading to a decrease in net flux. Thiocyanate, at 5 x 10(-3) or 5 x 10(-2) M, decreased active bicarbonate flux and hence net flux, but had no effect on sodium fluxes. Dinitrophenol increased only the passive bicarbonate flux while decreasing both active and passive sodium fluxes, albeit unequally, leading to a decreased net flux. Ethacrynic acid affected only passive bicarbonate flux, while decreasing net sodium flux. The stilbene derivatives, SITS and DIDS caused opposite effects on both sodium and bicarbonate fluxes. SITS decreased net bicarbonate flux by decreasing active and increasing passive flux, yet increased net sodium flux. DIDS, however, increased net bicarbonate flux but decreased net sodium flux. The results may be explained by current models for endothelial ion transport that include a Na+/H+ antiport and a HCO3-/Na+ symport system in parallel with an independent pathway for HCO3- exit from the endothelial cells. When compared with prior corneal swelling data using these same inhibitors, the maintenance of corneal thickness appears to be dependent on the variation of ion fluxes from normal values, and the dissociation of the two active ion fluxes. In addition, there appears to be a significant ability of ion transport systems to compensate for disturbances to other ion exchange or transport mechanisms.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2275927&dopt=Abstract
Naunyn Schmiedebergs Arch Pharmacol. 1986 Jul;333(3):323-9.
Inhibition of ion transport in Ehrlich cells by muzolimine.
Geck P, Pfeiffer B.
The influence of muzolimine on the transport of Na+, K+ and Cl- was studied in Ehrlich cells to test whether the diuretic inhibits the furosemide-sensitive Na+-K+-2 Cl-(-)cotransport or transport via the ouabain-sensitive Na+/K+-pump. It was shown that between 10(-5) M and 10(-3) M muzolimine pump-flux decreases with increasing drug concentration (IC50 about 0.5 mM), in contrast to the unaffected cotransport. This reduction in pump rate is only seen with respiring cells, but not during glycolytic ATP-production. Therefore, muzolimine seems to inhibit the Na+/K+-pump not directly but indirectly by interference with energy metabolism resulting in decreased ATP concentration. This reduction in ATP-level is at least partially due to activation of an ATP-consuming process of unknown nature. Whether muzolimine also inhibits respiration was not tested.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2429195&dopt=Abstract
J Clin Invest. 1988 Sep;82(3):1067-74.
Atrial natriuretic peptides inhibit conductive sodium uptake by rabbit inner medullary collecting duct cells.
Zeidel ML, Kikeri D, Silva P, Burrowes M, Brenner BM.
Renal Division, Brigham and Women's Hospital, Boston, Massachusetts 02115.
The inner medullary collecting duct (IMCD) effects net sodium reabsorption under the control of volume regulatory hormones, including atrial natriuretic peptides (ANP). These studies examined the mechanisms of sodium transport and its regulation by ANP in fresh suspensions of IMCD cells. Sodium uptake was inhibited by amiloride but insensitive to furosemide, bu-metanide, and hydrochlorthiazide. These results are consistent with uptake mediated by a sodium channel or Na+/H+ exchange. To determine the role of sodium channels, cells were hyperpolarized by preincubation in high potassium medium followed by dilution into potassium-free medium. Membrane potential measurements using the cyanine dye, Di(S)-C3-5 verified a striking hyperpolarization of IMCD cells using this protocol. Hyperpolarization increased the apparent initial rate of sodium uptake fourfold. Amiloride and ANP inhibited potential-stimulated sodium uptake 73% and 65%, respectively; the two agents together were not additive. Addition of 5 mM sodium to hyperpolarized cells resulted in a significant amiloride-sensitive depolarization. Half-maximal inhibition of potential-driven sodium uptake occurred at 3 X 10(-7) M amiloride, and 5 X 10(-11) M ANP. We conclude that sodium enters IMCD cells via a conductive, amiloride-sensitive sodium channel, which is regulated by ANP. ANP inhibition of luminal sodium entry in the IMCD appears to contribute to the marked natriuretic effect of this hormone in vivo.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2458385&dopt=Abstract
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