Inhibition of Na+/H+ exchange reduces Ca2+ mobilization without affecting the initial cleavage of phosphatidylinositol 4,5‐bisphosphate in thrombin‐stimulated platelets

Siffert, Winfried; Siffert, G.; Scheid, P.; Riemens, TI; Gorter, Gertie; Akkerman, J. W. N.

doi:10.1016/0014-5793(87)81569-7

Cited by 43 publications

(6 citation statements)

References 16 publications

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“…The data suggest that epinephrine-provoked stimulation of phospholipase-A activity may be preceded by intraplatelet alkalinization resulting from accelerated Na + / H + exchange (21). Similarly, blocking Na + /H + exchange by removal of extracellular Na + or by ethylisopropylamilofide inhibits calcium mobilization induced by 0.2 U/ ml thrombin in human platelets (22).…”

Section: Discussionmentioning

confidence: 99%

Lysophosphatidylinositol: A Potential Mediator of 1,25-Dihydroxyvitamin D-Induced Increments in Hepatocyte Cytosolic Calcium*

Baran

Kelly²

1988

Endocrinology

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Recent studies in our laboratory demonstrate that 1,25-dihydroxyvitamin D [1,25-(OH)2D] increases hepatocyte cytosolic calcium in the absence of extracellular calcium and activates phospholipase-A-induced deacylation of phosphatidylinositol within 5 min. To determine whether inhibition of phospholipase-A affects D-induced increments in cytosolic calcium and which metabolite of phosphatidylinositol mediates these increments, cytosolic calcium is measured in cultured hepatocytes, loaded with Fura 2AM. Cellular fluorescence is determined at excitation wavelengths of 340 and 380 nm, and cytosolic calcium is calculated. 1,25-(OH)2D treatment for 5 min increases cytosolic calcium levels in the cultured hepatocyte. Inhibition of phospholipase-A with bromophenacylbromide blocks the vitamin D effect on cytosolic calcium, indicating that phospholipase-A activation precedes increments in cytosolic calcium. Neither arachidonic acid nor sodium arachidonate affects cytosolic calcium. In contrast, LPI increases hepatocyte cytosolic calcium in the presence and absence of extracellular calcium. The effect is not blocked by bromophenacylbromide. Neither cell viability nor supernatant fluorescence is altered by LPI, indicating that LPI is increasing fluorescence within the cell. 1,25-(OH)2D treatment for 5 min increases cytosolic pH in cultured hepatocytes. Inhibition of cell alkalinization with amiloride blocks the vitamin D effect on both cytosolic pH and cytosolic calcium, but not the effect of LPI on calcium. NH4Cl increases hepatocyte pH but not cytosolic calcium. The results indicate that phospholipase-A activation is necessary for 1,25-(OH)2D-induced increments in hepatocyte cytosolic calcium and that LPI, a deacylation product of phosphatidylinositol, mediates these increments. Furthermore, inhibition of Na+/H+ exchange, while not blocking the ability of the cell to increase cytosolic calcium in response to LPI, prevents the 1,25-(OH)2D-induced increments in both pH and calcium. The data suggest that the rapid effects of 1,25-(OH)2D on hepatocyte calcium are preceded by cell alkalinization and phospholipase-A activation, and these effects appear to be linked to the Na+/H+ antiport system and not nonspecific cell alkalinization.

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Section: Discussionmentioning

confidence: 99%

Lysophosphatidylinositol: A Potential Mediator of 1,25-Dihydroxyvitamin D-Induced Increments in Hepatocyte Cytosolic Calcium*

Baran

Kelly²

1988

Endocrinology

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“…This ensures the cominuation of the cellular functions [14,14a, 15]. Both DAG and IP 3 are formed, indicating that only steps distal to their formation are affected [17]. Adding monesin, a known Na+/H + ionophore, reversed this inhibition.…”

Section: Discussionmentioning

confidence: 99%

The regulatory role of external cations on human polymorphonuclear phagocyte chemiluminescence

Janah

1990

FEMS Microbiology Letters

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The effect of the external cations Na+ and Ca2+ on polymorphonuclear chemiluminescence was investigated. Both Ca2+ in the range of 0.2–2 mM and Na+ in the range of 114–143 mM showed a dose dependent increase in polymorphonuclear chemiluminescence, irrespective of the concurrent increase in osmolality. The Na+/H+ antiport inhibitor Amiloride decreased the response significantly. These effects were observed using buffers commonly used for chemiluminescence studies and indicate the importance of defining the Ca2+ and Na+ composition of the buffers used in chemiluminescence assays.

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“…Adding monesin, a known Na+/H + ionophore, reversed this inhibition. Both DAG and IP 3 are formed, indicating that only steps distal to their formation are affected [17].…”

Section: Discussionmentioning

confidence: 99%

The regulatory role of external cations on human polymorphonuclear phagocyte chemiluminescence

Janah

Mali

Fleck

1990

FEMS Microbiology Letters

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SUMMARYThe effect of the external cations Na + and Ca 2+ on polymorphonuclear chemiluminescence was investigated. Both Ca 2+ in the range of 0.2-2 mM and Na + in the range of 114-I43 mM showed a dose dependent increase in polymorphonuclear chemiluminescence, irrespective of the concurrent increase in osmolality. The Na+/H + antiport inhibitor Amiloride decreased the response significantly. These effects were observed using buffers commonly used for chemiluminescence studies and indicate the importance of defming the Ca 2+ and Na + composition of the buffers used in chemiluminescence assays. 0920-8534/90/$03.50

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Inhibition of Na⁺/H⁺ exchange reduces Ca²⁺ mobilization without affecting the initial cleavage of phosphatidylinositol 4,5‐bisphosphate in thrombin‐stimulated platelets

Cited by 43 publications

References 16 publications

Lysophosphatidylinositol: A Potential Mediator of 1,25-Dihydroxyvitamin D-Induced Increments in Hepatocyte Cytosolic Calcium*

Lysophosphatidylinositol: A Potential Mediator of 1,25-Dihydroxyvitamin D-Induced Increments in Hepatocyte Cytosolic Calcium*

The regulatory role of external cations on human polymorphonuclear phagocyte chemiluminescence

The regulatory role of external cations on human polymorphonuclear phagocyte chemiluminescence

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