Circulation, Vol 88, 193-197, Copyright © 1993 by American Heart Association
M Ohno, GH Gibbons, VJ Dzau and JP Cooke
BACKGROUND. The endothelium acts as the sensor of shear stress and as the
mediator of flow-induced changes in vessel tone and structure. The purpose
of this study was to delineate the signal transduction pathway of
flow-induced release of endothelium-derived relaxing factor (EDRF). METHODS
AND RESULTS. We used a shear stress apparatus (a modified cone- plate
viscometer) to expose cultured endothelial cells to a well- defined laminar
fluid flow. Confluent bovine aortic endothelial cells (BAECs) were
subjected to varying levels of shear stress, and intracellular cyclic GMP
(cGMP) in the BAECs was measured by radioimmunoassay. After 60 seconds of
laminar fluid flow, BAEC cGMP increased by 300% from basal levels (from
0.54 to 1.70 pmol/mg protein, P < 0.05). The elevation in intracellular
cGMP was proportional to the intensity of shear stress within a
physiological range up to 40 dynes/cm2. This increase in cGMP was abrogated
by L-N-methyl-arginine (the competitive antagonist of nitric oxide [NO]
synthase), indicating that the flow-induced activation of soluble guanylate
cyclase was mediated by autocrine NO production. Furthermore, a potassium
channel antagonist, tetraethylammonium ion (TEA [3 mmol/L]) and a G(i) or
G(o) protein inhibitor, pertussis toxin (100 ng/mL) also blocked the flow-
induced increase in cGMP. By contrast, calcium ionophore or atrial
natriuretic peptide caused elevations of cGMP that were not affected by TEA
or pertussis toxin. CONCLUSIONS. These findings indicate that shear stress
elevates endothelial cGMP via an NO-dependent mechanism. The effect of
shear stress is mediated by a unique signal transduction pathway that is
coupled to a pertussis toxin-sensitive G protein and that requires the
activity of an endothelial potassium channel.
ARTICLES
Shear stress elevates endothelial cGMP. Role of a potassium channel and G protein coupling
Division of Cardiovascular Medicine, Stanford University School of Medicine, Calif.
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