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1 Department of Pathophysiology, Semmelweis University of Medicine, H-1445 Budapest, Hungary; and 2 Department of Physiology, New York Medical College, Valhalla, New York 10595
In cultured endothelial cells, Ca2+-dependent and
-independent activation of nitric oxide (NO) synthesis to agonists and
flow/wall shear stress (WSS) has been demonstrated. However, the
presence and function of these pathways are less well known in
microvessels that can be exposed to a high level of WSS. We
hypothesized that the role of changes in endothelial intracellular
calcium concentration ([Ca2+]i) is different
in agonist- and WSS-induced release of NO. Thus changes in endothelial
[Ca2+]i and diameter of intact pressurized
(~100 µm at 80 mmHg) gracilis skeletal muscle arterioles of rats
were measured by fluorescent videomicroscopy. Acetylcholine (ACh) and
increases in WSS (by increasing intraluminal flow) elicited dilations
(maximum 91 ± 2% and 34 ± 4%) that could be inhibited by
N
-nitro-L-arginine methyl ester
(L-NAME), a NO synthase blocker. In diameter-clamped
arterioles, ACh caused substantial increases in the endothelial calcium
fluorescence ratio (ERCa, maximum 43 ± 5%), which
was significantly greater than changes in ERCa (maximum ~10%) to increases in WSS. The Ca2+ ionophore A-23187
also substantially increased ERCa (maximum 38 ± 5%)
and elicited significant L-NAME-sensitive arteriolar dilations (maximum 45 ± 7%). Intraluminal administration of the tyrosine kinase inhibitor genistein had no effect on dilations induced
by ACh or the NO donor sodium nitroprusside, whereas it eliminated
WSS-induced dilations. Collectively, our data suggest that, in
endothelium of skeletal muscle arterioles, NO synthesis is activated by
shear stress without a substantial increase in [Ca2+]i, most likely by activation of
tyrosine kinase pathways, whereas NO release by ACh and A-23187 is
associated with substantial increases in
[Ca2+]i.
fura 2; endothelial calcium fluorescence ratio; calcium-independent pathways; tyrosine kinase; endothelium-derived hyperpolarizing factor
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