DIDS inhibition of deformation-induced cation flux in human erythrocytes

Johnson, Robert M.; Tang, Ke

doi:10.1016/0005-2736(93)90154-r

Cited by 14 publications

(6 citation statements)

References 41 publications

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“…2 We have suggested that the pathway reflects the activity of a nonselective cation channel, activated by the membrane distortion associated with sickling. Many of the characteristics of sickling-induced cation fluxes, including inhibition by DIDS, 29 are shared by the passive cation leaks induced by high shear stress in normal and sickle RBCs. 30 Recently, we described single ion channels in membrane vesicles derived from the spectrin-depleted spicules of sickled RBCs.…”

Section: Discussionmentioning

confidence: 99%

Dipyridamole inhibits sickling-induced cation fluxes in sickle red blood cells

Joiner

Jiang

Claussen

et al. 2001

Blood

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Section: Discussionmentioning

confidence: 99%

Dipyridamole inhibits sickling-induced cation fluxes in sickle red blood cells

Joiner

Jiang

Claussen

et al. 2001

Blood

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“…In sum, these results can be interpreted as evidence that oxidation increases the sensitivity of the cell to mem-200 400 600 800 1000 1200 1400 applied stress (dynes/cm 2 ) brane tension. Anion exchange is not affected by mechanical shear (Johnson and Tang, 1993).…”

Section: Elmentioning

confidence: 93%

Membrane stress increases cation permeability in red cells

Johnson

1994

Biophysical Journal

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The human red cell is known to increase its cation permeability when deformed by mechanical forces. Light-scattering measurements were used to quantitate the cell deformation, as ellipticity under shear. Permeability to sodium and potassium was not proportional to the cell deformation. An ellipticity of 0.75 was required to increase the permeability of the membrane to cations, and flux thereafter increased rapidly as the limits of cell extension were reached. Induction of membrane curvature by chemical agents also did not increase cation permeability. These results indicate that membrane deformation per se does not increase permeability, and that membrane tension is the effector for increased cation permeability. This may be relevant to some cation permeabilities observed by patch clamping.

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“…The anion exchanger 1 (AE1), a major structural membrane component that also mediates chloride–bicarbonate exchange may play a crucial role in this. Normal RBCs demonstrate a (likely AE1-mediated) cation leak when undergoing shear stress,13 and AE1 is the proposed mediator of deoxygenation-induced cation-selective channel (P sickle ) cation flux 14. When compared with normal RBCs, sickle RBCs demonstrate an exaggerated potassium leak in response to shear stress, which is further enhanced at lower pHs 15.…”

Section: Putative Modelmentioning

confidence: 99%