Hypertension, Vol 21, 112-127, Copyright © 1993 by American Heart Association
HM Himmel, AR Whorton and HC Strauss
Vascular endothelium appears to be a unique organ. It not only responds to
numerous hormonal and chemical signals but also senses changes in physical
parameters such as shear stress, producing mediators that modulate the
responses of numerous cells, including vascular smooth muscle, platelets,
and leukocytes. In many cases, the initial response of endothelial cells to
these diverse signals involves elevation of cytosolic Ca2+ and activation
of Ca(2+)-dependent enzymes, including nitric oxide synthase and
phospholipase A2. Both the release of Ca2+ from intracellular stores, most
likely the endoplasmic reticulum, and the influx of Ca2+ from the
extracellular space contribute to the [Ca2+]i increase. The most important
trigger for Ca2+ release is inositol 1,4,5-trisphosphate, which is
generated by the action of phospholipase C, a plasmalemmal enzyme activated
in many cases by the receptor-G protein cascade. Ca2+ influx appears to be
related to the activity of receptor-G protein-enzyme complex and to the
degree of fullness of the endoplasmic reticulum but does not involve
voltage- gated Ca2+ channels. The magnitude of the Ca2+ influx depends on
the electrochemical gradient, which is modulated by the membrane potential,
Vm. Under basal conditions, Vm is dominated by a large inward rectifier K+
current. Some stimuli, e.g., acetylcholine, have been shown to
hyperpolarize Vm, thus increasing the electrochemical gradient for Ca2+,
which appears to be modulated by activation of Ca(2+)-dependent K+ and Cl-
currents. However, the lack of potent and specific blockers for many of the
described or postulated channels (e.g., nonselective cation channel,
Ca(2+)-activated Cl- channel) makes an estimation of their effect on
endothelial cell function rather difficult. Possible future directions of
research and clinical implications are discussed.
ARTICLES
Intracellular calcium, currents, and stimulus-response coupling in endothelial cells
Department of Pharmacology, Duke University Medical Center, Durham, N.C. 27710.
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