The use of ionophores of rapid loading of human red cells with radioactive cations for cation-pump studies

Sarkadi, Balázs; Szász, I; Gárdos, George

doi:10.1007/bf01868883

Cited by 124 publications

(30 citation statements)

References 26 publications

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“…However, the initial K ϩ efflux, which occurs before there is substantial cell lysis, is likely to cause the extensive volume reduction seen in the early phases of HlyA-induced hemolysis. This resembles what has been observed with Ca 2ϩ ionophores (17,24). A good candidate for an activated K ϩ efflux pathway is the K Ca 3.1 channel (SK 4 or Gardos channel); the only Ca 2ϩ -activated K ϩ channel known to be present in erythrocytes (25,26).…”

Section: Discussionsupporting

confidence: 87%

Escherichia coli α-Hemolysin Triggers Shrinkage of Erythrocytes via KCa3.1 and TMEM16A Channels with Subsequent Phosphatidylserine Exposure

Skals

Jensen

Ousingsawat

et al. 2010

Journal of Biological Chemistry

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Section: Discussionsupporting

confidence: 87%

Escherichia coli α-Hemolysin Triggers Shrinkage of Erythrocytes via KCa3.1 and TMEM16A Channels with Subsequent Phosphatidylserine Exposure

Skals

Jensen

Ousingsawat

et al. 2010

Journal of Biological Chemistry

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“…It is apparent that A23187-induced cyclic GMP production is less in the presence of SOD or SOD and CAT than in their absence (cf Table 5 and Figure 4). This may well reflect protein binding of the ionophore, as A23187 is known to bind to albumin: indeed binding of A23187 to albumin has been used as a technique for rapid removal and reversal of the effects of A23187 (Sarkadi et al, 1976).…”

Section: Discussionmentioning

confidence: 99%

Release of endothelium‐derived relaxing factor from pig cultured aortic endothelial cells, as assessed by changes in endothelial cell cyclic GMP content, is inhibited by a phorbol ester

Smith

Lang

1990

British J Pharmacology

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Cultured aortic endothelial cells of the pig respond to the endothelium‐derived relaxing factor (EDRF) they release with an increase in cyclic GMP content. This response is inhibited by haemoglobin or by l‐NG‐monomethyl‐arginine (l‐NMMA), and has been used to investigate the effects of phorbol esters on EDRF release. Pretreatment with phorbol‐12,13‐dibutyrate (PDB) but not the inactive 4α‐phorbol‐12,13,‐didecanoate (PDD), inhibited increases in cyclic GMP induced by substance P (10−8 m) in a time and concentration‐dependent manner. PDB did not affect basal cyclic GMP levels. PDB (3 × 10−7 m), but not PDD (3 × 10−7 m), also inhibited ATP (10−5 m)‐induced increases in cyclic GMP, but did not affect those induced by bradykinin (10−7 m). Increases in cyclic GMP induced by low (10−7 m) but not high (10−6 m) concentrations of the calcium ionophore A23187 were inhibited by PDB (3 × 10−7 m). This inhibitory effect was due to enhanced destruction of EDRF by superoxide anions rather than inhibition of EDRF release, as the inhibition was abolished in the presence of superoxide dismutase (SOD, 30 u ml−1) and catalase (CAT, 100 u ml−1). SOD and CAT did not affect the inhibitory action of PDB on substance P or ATP‐induced increases in cyclic GMP. Increases in endothelial cell cyclic GMP content induced by sodium nitroprusside (10−5 m) were unaffected by PDB pretreatment. The inhibitory effects of PDB are probably a result of an action of protein kinase C on the steps between receptor occupation and phospholipase C activation.

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“…Trapped PBS was estimated by tagging the solution with '"IHSA (0.15 MCi/ml). The water content was estimated by drying the sample at 1050C to a constant weight (generally within [24][25][26][27][28][29][30][31][32][33][34][35][36] h). This value was corrected for the trapped PBS solution.…”

Section: Methodsmentioning

confidence: 99%

“…Theoretically, PTH may also promote calcium entry into RBC, and it has been shown that small increases in intracellular calcium of RBC evoked crenation and increased rigidity (20)(21)(22)(23)(24). Thus, excess blood levels of PTH in patients with uremia could be, at least in part, responsible for the reduced survival of RBC in these patients.…”

mentioning

confidence: 99%

Effect of Parathyroid Hormone on Osmotic Fragility of Human Erythrocytes

Bogin¹,

Massry²,

Levi³

et al. 1982

J. Clin. Invest.

185

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A B S T R A C T The survival of erythrocytes (RBC) is shortened in uremia, and it has been shown that calcium influx into RBC evoked crenation and increased their rigidity. The high blood levels of parathyroid hormone (PTH) may augment entry of calcium into RBC and hence affect their integrity. We examined the effect of PTH on osmotic fragility of human RBC and investigated the mechanisms through which PTH interacts with RBC. Both the amino-terminal (1-34) PTH and the intact (1-84) PTH, but not the carboxy-terminal (53-84) PTH, produced significant increases in osmotic fragility. This effect was abolished by prior inactivation of the hormone. There was a dose-response relationship between both moieties of PTH and the increase in osmotic fragility. This action of PTH required calcium, was mimicked by calcium ionophore, and was partially blocked by verapamil. PTH caused significant influx of 45Ca into RBC, which was not associated with potassium leak. The hormone did not affect water content of RBC. Scanning electron microscopy revealed that the incubation of RBC with PTH was associated with the appearance of membrane filamentous extensions, which anchor RBC together.Inhibition of glycolytic activity of RBC with NaF or inhibition of Na-K-activated ATPase with ouabain did not abolish the effect of PTH on osmotic fragility. PTH did not stimulate RBC Na-K-activated ATPase or Mg-dependent ATPase but caused marked and significant stimulation of Ca-activated ATPase. The basal activity of the RBC adenylate cyclase was low and PTH produced only a modest stimulation of this enzyme. Both cyclic AMP and dibutyryl cyclic AMP had no effect on osmotic fragility.The data indicate that: (a) the RBC is a target organ for PTH, (b) the hormone increases osmotic fragility

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The use of ionophores of rapid loading of human red cells with radioactive cations for cation-pump studies

Cited by 124 publications

References 26 publications

Escherichia coli α-Hemolysin Triggers Shrinkage of Erythrocytes via KCa3.1 and TMEM16A Channels with Subsequent Phosphatidylserine Exposure

Escherichia coli α-Hemolysin Triggers Shrinkage of Erythrocytes via KCa3.1 and TMEM16A Channels with Subsequent Phosphatidylserine Exposure

Release of endothelium‐derived relaxing factor from pig cultured aortic endothelial cells, as assessed by changes in endothelial cell cyclic GMP content, is inhibited by a phorbol ester

Effect of Parathyroid Hormone on Osmotic Fragility of Human Erythrocytes

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