Am J Physiol Cell Physiol AJP: Cell Physiology
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Am J Physiol Cell Physiol (May 15, 2002). doi:10.1152/ajpcell.00057.2002
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Articles in PresS, published online ahead of print May 10, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00057.2002
Submitted on February 7, 2002
Accepted on April 9, 2002

Stretch-induced Ca2+ release via an IP3 insensitive Ca2+ channel

Madhumita Jena Mohanty1* and Xingli Li1

1 Internal Medicine, Wayne State University School of Medicine, Detroit, MI, USA; Internal Medicine, John D Dingell VA Medical Center, Detroit, MI, USA

* To whom correspondence should be addressed. E-mail: jenam{at}intmed.wayne.edu.

Various mechanical stimuli increase the intracellular calcium concentration ([Ca2+]i) in vascular smooth muscle cells (VSMC). A part of the increase in [Ca2+]i is due to the release of calcium (Ca2+) from the intracellular stores. We have investigated the effect of mechanical stimulation produced by cyclical stretch on the release of Ca2+ from the intracellular stores. Permeabilized VSMC loaded with 45Ca2+ were subjected to 7.5% average (15% maximal) cyclical stretch. This resulted in an increase in 45Ca2+ rate constant by 0.126 ± 0.0035. Inhibition of inositol 1,4,5-triphosphate (IP3), ryanodine and nicotinic acid adenine dinucleotide phosphate channels (NAADP) with 50 µg/ml heparin, 50 µM ruthenium red and 25 µM thioNADP respectively did not block the increase in 45Ca2+ efflux in response to cyclical stretch. However, 10 µM lanthanum, 10 µM gadolinium and 10 µM cytochalasin D but not 10 µM nocodazole inhibited the increase in 45Ca2+ efflux. This supports the existence of a novel stretch-sensitive intracellular Ca2+ store in VSMC that is distinct from the IP3, ryanodine and NAADP sensitive stores.




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