Appendix to Calcium Exchange in the Heart

1983 ◽  
pp. 467-469
Author(s):  
G. A. Langer
Keyword(s):  
Calcium Exchange

scholarly journals Lithium-Calcium Exchange Is Mediated by a Distinct Potassium-independent Sodium-Calcium Exchanger

2004 ◽  
Vol 279 (24) ◽  
pp. 25234-25240 ◽  
Author(s):  
Raz Palty ◽  
Ehud Ohana ◽  
Michal Hershfinkel ◽  
Micha Volokita ◽  
Vered Elgazar ◽  
...  
Keyword(s):  
Sodium Calcium Exchanger ◽  
Sodium Calcium ◽  
Calcium Exchange

Calcitropic gene expression suggests a role for the intraplacental yolk sac in maternal-fetal calcium exchange

2002 ◽  
Vol 282 (3) ◽  
pp. E721-E732 ◽  
Author(s):  
Christopher S. Kovacs ◽  
Linda L. Chafe ◽  
Mandy L. Woodland ◽  
Kirsten R. McDonald ◽  
Neva J. Fudge ◽  
...  
Keyword(s):  
Time Frame ◽  
Yolk Sac ◽  
Late Gestation ◽  
Calcium Sensing ◽  
Parathyroid Hormone Related Protein ◽  
Active Calcium ◽  
Calcium Exchange ◽  
Calbindin D ◽  
Pthrp Receptor

The expression of calcitropic genes and proteins was localized within murine placenta during late gestation (the time frame of active calcium transfer) with an analysis of several gene-deletion mouse models by immunohistochemistry and in situ hybridization. Parathyroid hormone-related protein (PTHrP), the PTH/PTHrP receptor, calcium receptor, calbindin-D9k, Ca2+-ATPase, and vitamin D receptor were all highly expressed in a localized structure of the murine placenta, the intraplacental yolk sac, compared with trophoblasts. In the PTHrP gene-deleted or Pthrp-null placenta in which placental calcium transfer is decreased, calbindin-D9k expression was downregulated in the intraplacental yolk sac but not in the trophoblasts. These observations indicated that the intraplacental yolk sac contains calcium transfer and calcium-sensing capability and that it is a probable route of maternal-fetal calcium exchange in the mouse.

Sodium-calcium exchange-mediated contractions in feline ventricular myocytes

1992 ◽  
Vol 263 (4) ◽  
pp. H1161-H1169 ◽  
Author(s):  
H. B. Nuss ◽  
S. R. Houser
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Ventricular Myocytes ◽  
Membrane Potentials ◽  
Exchange Mechanism ◽  
Ca Channel ◽  
Ca Current ◽  
Voltage Step ◽  
Reverse Mode ◽  
Sodium Calcium ◽  
Calcium Exchange

The hypothesis that Ca entry by the sarcolemmal Na-Ca exchange mechanism induces sarcoplasmic reticulum (SR) Ca release, loads the SR with Ca, and/or directly induces contractions by elevating cytosolic free Ca was tested in voltage-clamped feline ventricular myocytes. Intracellular Na concentration was increased by cellular dialysis to enhance Ca influx via "reverse-mode" Na-Ca exchange at positive membrane potentials, at which the "L-type" Ca current (ICa) should be small. Contractions were induced in the presence of Ca channel antagonists by depolarization to these potentials, suggesting that Ca influx via reverse-mode Na-Ca exchange was involved. These contractions had both phasic (SR related) and tonic components of shortening. They were smaller and began with more delay after depolarization than contractions which involved ICa. The magnitude of shortening was graded by the amount and duration of depolarization, suggesting that Ca influx via reverse-mode Na-Ca exchange has the capacity to induce and grade SR Ca release. Small slow contractions could be evoked in the presence of ryanodine (to impair SR function) and verapamil (to block ICa), supporting the idea that Ca influx via Na-Ca exchange is sufficient to directly activate the contractile proteins. Contractions induced by voltage steps to +10 mV, which were usually small when ICa was blocked, were potentiated if preceded by a voltage step to strongly positive potentials. This potentiation was inhibited by ryanodine, suggesting that Ca entry that occurs by Na-Ca exchange may be important for normal SR Ca loading.(ABSTRACT TRUNCATED AT 250 WORDS)

Cellular Regulation of Sodium-Calcium Exchange

2006 ◽  
Vol 976 (1) ◽  
pp. 214-223 ◽  
Author(s):  
MADALINA CONDRESCU ◽  
KWABENA OPUNI ◽  
BASIL M. HANTASH ◽  
JOHN P. REEVES
Keyword(s):  
Cellular Regulation ◽  
Sodium Calcium ◽  
Calcium Exchange ◽  
Sodium Calcium Exchange

Doubling time α-aminoisobutyrate transport and calcium exchange in cultured fibroblasts from cystic fibrosis and control subjects

1978 ◽  
Vol 82 (1-2) ◽  
pp. 125-131 ◽  
Author(s):  
Burton L. Shapiro ◽  
Robert J. Feigal ◽  
Nancy J. Laible ◽  
Michelle H. Biros ◽  
Warren J. Warwick
Keyword(s):  
Cystic Fibrosis ◽  
Doubling Time ◽  
Cultured Fibroblasts ◽  
Control Subjects ◽  
Calcium Exchange ◽  
And Control

Inhibition of sodium-calcium exchange in cardiac sarcolemmal membrane vesicles. 1. Mechanism of inhibition by amiloride analogs

Biochemistry ◽  
1988 ◽  
Vol 27 (7) ◽  
pp. 2403-2409 ◽  
Author(s):  
Robert S. Slaughter ◽  
Maria L. Garcia ◽  
Edward J. Cragoe ◽  
John P. Reeves ◽  
Gregory J. Kaczorowski
Keyword(s):  
Membrane Vesicles ◽  
Sarcolemmal Membrane ◽  
Sodium Calcium ◽  
Mechanism Of Inhibition ◽  
Calcium Exchange ◽  
Sodium Calcium Exchange ◽  
Amiloride Analogs

scholarly journals Erythrocyte calcium metabolism. Calcium exchange in normal and sickle-cell-anaemia erythrocytes

1976 ◽  
Vol 156 (3) ◽  
pp. 577-583 ◽  
Author(s):  
B F Cameron ◽  
P E Smariga
Keyword(s):  
Sickle Cell ◽  
Calcium Metabolism ◽  
Sickle Cell Anaemia ◽  
Similar Proportion ◽  
Exchange Equilibrium ◽  
Exchangeable Calcium ◽  
Calcium Loading ◽  
Calcium Exchange ◽  
Phosphate Buffered Saline ◽  
Calcium Pool

Under exchange conditions (no net increase in calcium), erythrocytes incubated in isoosmotic phosphate-buffered saline have an exchangeable calcium pool comprising about 10% of the total erythrocyte calcium. This pool reaches exchange equilibrium, for either inward-directed or outward-directed transfer of the 45Ca-exchange label, with a half-time of about 20 min. The uptake of Ca2+ requires phosphate, even under hypo-osmotic conditions, where the calcium loading expected as the cells swell is obtained only when phosphate is present. The phosphate requirement is not due to Ca2+ transport as a phosphate salt. This exchangeable-calcium pool is also present in sickle-cell-anemia erythrocytes, and comprises a similar proportion of total cellular calcium.

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