Role of Intracellular Calcium in the Regulation of Renal Hemodynamics

In fura 2-loaded N1E-115 cells, regulation of intracellular Ca2+ concentration ([Ca2+]i) following a Ca2+ load induced by 1 μM thapsigargin and 10 μM carbonylcyanide p-trifluoromethyoxyphenylhydrazone (FCCP) was Na+ dependent and inhibited by 5 mM Ni2+. In cells with normal intracellular Na+ concentration ([Na+]i), removal of bath Na+, which should result in reversal of Na+/Ca2+exchange, did not increase [Ca2+]i unless cell Ca2+ buffer capacity was reduced. When N1E-115 cells were Na+ loaded using 100 μM veratridine and 4 μg/ml scorpion venom, the rate of the reverse mode of the Na+/Ca2+ exchanger was apparently enhanced, since an ∼4- to 6-fold increase in [Ca2+]ioccurred despite normal cell Ca2+ buffering. In SBFI-loaded cells, we were able to demonstrate forward operation of the Na+/Ca2+ exchanger (net efflux of Ca2+) by observing increases (∼ 6 mM) in [Na+]i. These Ni2+ (5 mM)-inhibited increases in [Na+]i could only be observed when a continuous ionomycin-induced influx of Ca2+ occurred. The voltage-sensitive dye bis-(1,3-diethylthiobarbituric acid) trimethine oxonol was used to measure changes in membrane potential. Ionomycin (1 μM) depolarized N1E-115 cells (∼25 mV). This depolarization was Na+dependent and blocked by 5 mM Ni2+ and 250–500 μM benzamil. These data provide evidence for the presence of an electrogenic Na+/Ca2+ exchanger that is capable of regulating [Ca2+]i after release of Ca2+ from cell stores.

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Physiologic Role of ETA Receptors in the Regulation of Renal Hemodynamics in Normal and Salt-Depleted Rats

Journal of Cardiovascular Pharmacology ◽

10.1097/00005344-199506263-00137 ◽

1995 ◽

Vol 26 ◽

pp. S466-469 ◽

Cited By ~ 3

Author(s):

Clarice Kazue Fujihara ◽

Gilberto De Nucci ◽

Roberto Zatz

Keyword(s):

Renal Hemodynamics ◽

Physiologic Role

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The role of intracellular calcium phosphate in osteoblast-mediated bone apatite formation

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1208916109 ◽

2012 ◽

Vol 109 (35) ◽

pp. 14170-14175 ◽

Cited By ~ 269

Author(s):

S. Boonrungsiman ◽

E. Gentleman ◽

R. Carzaniga ◽

N. D. Evans ◽

D. W. McComb ◽

...

Keyword(s):

Calcium Phosphate ◽

Intracellular Calcium ◽

Apatite Formation ◽

Bone Apatite

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Intracellular calcium levels in the Plasmodium berghei ookinete

Parasitology ◽

10.1017/s0031182008004939 ◽

2008 ◽

Vol 135 (12) ◽

pp. 1355-1362 ◽

Cited By ~ 6

Author(s):

I. SIDÉN-KIAMOS ◽

C. LOUIS

Keyword(s):

Intracellular Calcium ◽

Plasmodium Berghei ◽

Calcium Concentration ◽

Insect Cells ◽

Ionophore A23187 ◽

Rodent Malaria Parasite ◽

Calcium Indicators ◽

Intracellular Ca

SUMMARYOokinetes are the motile and invasive stages of Plasmodium parasites in the mosquito host. Here we explore the role of intracellular Ca2+ in ookinete survival and motility as well as in the formation of oocysts in vitro in the rodent malaria parasite Plasmodium berghei. Treatment with the Ca2+ ionophore A23187 induced death of the parasite, an effect that could be prevented if the ookinetes were co-incubated with insect cells before incubation with the ionophore. Treatment with the intracellular calcium chelator BAPTA/AM resulted in increased formation of oocysts in vitro. Calcium imaging in the ookinete using fluorescent calcium indicators revealed that the purified ookinetes have an intracellular calcium concentration in the range of 100 nm. Intracellular calcium levels decreased substantially when the ookinetes were incubated with insect cells and their motility was concomitantly increased. Our results suggest a pleiotropic role for intracellular calcium in the ookinete.

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Cytolysis mediated by ionophores and pore‐forming agents: role of intracellular calcium in apoptosis

The FASEB Journal ◽

10.1096/fasebj.8.2.8119494 ◽

1994 ◽

Vol 8 (2) ◽

pp. 237-246 ◽

Cited By ~ 77

Author(s):

Richard C. Duke ◽

Roxana Z. Witter ◽

Paul B. Nash ◽

John Ding‐E. Young ◽

David M. Ojcius

Keyword(s):

Intracellular Calcium

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Role of EP2 and EP3 PGE2receptors in control of murine renal hemodynamics

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.2001.280.1.h327 ◽

2001 ◽

Vol 280 (1) ◽

pp. H327-H333 ◽

Cited By ~ 37

Author(s):

Laurent P. Audoly ◽

Xiaoping Ruan ◽

Victoria A. Wagner ◽

Jennifer L. Goulet ◽

Stephen L. Tilley ◽

...

Keyword(s):

Renal Artery ◽

Vascular Reactivity ◽

Renal Hemodynamics ◽

Receptor Subtypes ◽

Male Mice ◽

Unique Role ◽

Arterial Blood ◽

Renal Vascular

The kidney plays a central role in long-term regulation of arterial blood pressure and salt and water homeostasis. This is achieved in part by the local actions of paracrine and autacoid mediators such as the arachidonic acid-prostanoid system. The present study tested the role of specific PGE2 E-prostanoid (EP) receptors in the regulation of renal hemodynamics and vascular reactivity to PGE2. Specifically, we determined the extent to which the EP2 and EP3 receptor subtypes mediate the actions of PGE2 on renal vascular tone. Renal blood flow (RBF) was measured by ultrasonic flowmetry, whereas vasoactive agents were injected directly into the renal artery of male mice. Studies were performed on two independent mouse lines lacking either EP2or EP3 (−/−) receptors and the results were compared with wild-type controls (+/+). Our results do not support a unique role of the EP2 receptor in regulating overall renal hemodynamics. Baseline renal hemodynamics in EP2−/− mice [RBF EP2−/−: 5.3 ± 0.8 ml · min−1 · 100 g kidney wt−1; renal vascular resistance (RVR) 19.7 ± 3.6 mmHg · ml−1 · min · g kidney wt] did not differ statistically from control mice (RBF +/+: 4.0 ± 0.5 ml · min−1 · 100 g kidney wt−1; RVR +/+: 25.4 ± 4.9 mmHg · ml−1 · min · 100 g kidney wt−1). This was also the case for the peak RBF increase after local PGE2 (500 ng) injection into the renal artery (EP2−/−: 116 ± 4 vs. +/+: 112 ± 2% baseline RBF). In contrast, we found that the absence of EP3receptors in EP3−/− mice caused a significant increase (43%) in basal RBF (7.9 ± 0.8 ml · min−1 · g kidney wt−1, P < 0.05 vs. +/+) and a significant decrease (41%) in resting RVR (11.6 ± 1.4 mmHg · ml−1 · min · g kidney wt−1, P < 0.05 vs. +/+). Local administration of 500 ng of PGE2 into the renal artery caused more pronounced renal vasodilation in EP3−/− mice (128 ± 2% of basal RBF, P < 0.05 vs. +/+). We conclude that EP3 receptors mediate vasoconstriction in the kidney of male mice and its actions are tonically active in the basal state. Furthermore, EP3receptors are capable of buffering PGE2-mediated renal vasodilation.

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