This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Tanaka, H. Articles by Takamatsu, T. Search for Related Content PubMed PubMed Citation Articles by Tanaka, H. Articles by Takamatsu, T. Related Collections Cell signalling/signal transduction Ion channels/membrane transport Endothelium/vascular type/nitric oxide

(Circulation Research. 2001;88:852.)
© 2001 American Heart Association, Inc.

Editorial

Calcium Spots

Elementary Signals in Response to Mechanical Stress in Vascular Endothelial Cells

Hideo Tanaka, Tetsuro Takamatsu

From the Department of Pathology and Cell Regulation, Kyoto Prefectural University of Medicine, Kyoto, Japan.

Correspondence to Dr Tetsuro Takamatsu, Professor of Pathology and Medicine, Kyoto Prefectural University of Medicine, Kawaramachi-Hirokoji, Kamikyo-Ku, Kyoto 6 02-0841, Japan. E-mail ttakam@basic.kpu-m.ac.jp

Key Words: endothelium • mechanotransduction • calcium • lysophosphatidic acid • confocal microscopy

	Introduction

 
Blood flow–mediated mechanical force, ie, shear stress, plays an important role in regulation of vascular function and development of various cardiovascular diseases.^{1 2 3} It directly stimulates vascular endothelial cells to mobilize intracellular Ca²⁺ ([Ca²⁺]_i), resulting in production of endothelium-derived vasoactive substances, such as nitric oxide and prostacyclin, which cause vasodilation by acting on smooth muscle cells.^{1 2 3} In this process, the mechanosensitive (MS) channel is an important pathway mediating the shear stress–induced increase in [Ca²⁺]_i.^{4 5 6 7} In addition, a specific vasoactive agonist, ATP, has been regarded as an important shear transducer of the endothelial [Ca²⁺]_i mobilization in response to fluid flow.^{8 9 10 11} Which initiates and mainly contributes to the [Ca²⁺]_i mobilization, MS channel or the shear transducer? The mechanism underlying the flow-induced [Ca²⁺]_i mobilization is controversial. Furthermore, little is known about the spatiotemporal properties of [Ca²⁺]_i mobilization triggered by MS channels or by the shear transducers.

In this issue of Circulation Research, Ohata et al¹² demonstrate novel spatiotemporal changes in [Ca²⁺]_i in response to fluid flow in cultured bovine aortic endothelial cells under the application of lysophosphatidic acid (LPA),^{13 14} a bioactive phospholipid. Using real-time confocal microscopy equipped with a multipinhole Nipkow disk–type scanner, it was shown that superfusion of the cells with LPA at physiologically relevant concentrations and flow rates produced spot-like elevations of [Ca²⁺]_i, ie, Ca²⁺ spots, which were localized to a circular area (<4 µm diameter), followed by gradual and concentric spread throughout the cells. The Ca²⁺ spots develop sporadically . . . [Full Text of this Article]