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Department of Physiology, New York Medical College, Valhalla, New York 10595
Previously, we frequently observed dilation of
arterioles after agonist-induced constrictions. We hypothesized that
deformation of the endothelium during decreases in diameter of isolated
arterioles elicits the release of nitric oxide (NO). In isolated
arterioles of rat mesentery, phenylephrine (PE, 10
7 M)-,
U-46619 (107 M)-, and KCl (50 mM)-induced constrictions
were followed by potent dilations. Inhibition of NO synthase with
N
-nitro-L-arginine
(L-NNA, 2 × 104 M) or removal of the
endothelium significantly enhanced constriction and reduced the
postconstriction dilation. In the presence of 80 mmHg of intraluminal
pressure, an increase in extraluminal pressure (Pe) to 75 mmHg for 20 s and 1 and 2 min decreased vessel diameter. After
release of Pe, arterioles dilated as a function of the
duration of diameter reduction by Pe. Removal of the
endothelium or administration of L-NNA significantly
diminished the post-Pe dilations. In cultured mesenteric
arteriolar endothelial cells (EC), PE, U-46619, or KCl did not
increase, whereas ACh did increase, the production of NO, as measured
by a fluorometric assay for nitrite. Furthermore, when EC, cultured on
a stretched silicone membrane, were subjected to deformation by
shortening the membrane to 50% of its original length, NO release
increased significantly. Based on all of the above, we propose that
deformation of EC per se elicits release of NO, a mechanism that
modulates arteriolar constriction.
arterioles; dilation; deformation of endothelium; mesentery; cell culture
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