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Comparative Capacitative Calcium Entry Mechanisms in Canine Pulmonary and Renal Arterial Smooth Muscle Cells
Author(s) -
Wilson Sean M.,
Mason Helen S.,
Smith Gregory D.,
Nicholson Neil,
Johnston Louise,
Janiak Robert,
Hume Joseph R.
Publication year - 2002
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2002.021998
Subject(s) - calcium , smooth muscle , medicine , chemistry , cardiology , anatomy
Experiments were performed to determine whether capacitative Ca 2+ entry (CCE) can be activated in canine pulmonary and renal arterial smooth muscle cells (ASMCs) and whether activation of CCE parallels the different functional structure of the sarcoplasmic reticulum (SR) in these two cell types. The cytosolic [Ca 2+ ] was measured by imaging fura‐2‐loaded individual cells. Increases in the cytosolic [Ca 2+ ] due to store depletion in pulmonary ASMCs required simultaneous depletion of both the inositol 1,4,5‐trisphosphate (Ins P 3 )‐ and ryanodine (RY)‐sensitive SR Ca 2+ stores. In contrast, the cytosolic [Ca 2+ ] rises in renal ASMCs occurred when the SR stores were depleted through either the Ins P 3 or RY pathways. The increase in the cytosolic [Ca 2+ ] due to store depletion in both pulmonary and renal ASMCs was present in cells that were voltage clamped and was abolished when cells were perfused with a Ca 2+ ‐free bathing solution. Rapid quenching of the fura‐2 signal by 100 μM Mn 2+ following SR store depletion indicated that extracellular Ca 2+ entry increased in both cell types and also verified that activation of CCE in pulmonary ASMCs required the simultaneous depletion of the Ins P 3 ‐ and RY‐sensitive SR Ca 2+ stores, while CCE could be activated in renal ASMCs by the depletion of either of the Ins P 3 ‐ or RY‐sensitive SR stores. Store depletion Ca 2+ entry in both pulmonary and renal ASMCs was strongly inhibited by Ni 2+ (0.1–10 mM), slightly inhibited by Cd 2+ (200–500 μM), but was not significantly affected by the voltage‐gated Ca 2+ channel (VGCC) blocker nisoldipine (10 μM). The non‐selective cation channel blocker Gd 3+ (100 μM) inhibited a portion of the Ca 2+ entry in 6 of 18 renal but not pulmonary ASMCs. These results provide evidence that SR Ca 2+ store depletion activates CCE in parallel with the organization of intracellular Ca 2+ stores in canine pulmonary and renal ASMCs.