title: Nitric oxide-mediated arteriolar dilation after endothelial deformation.
abstract: 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 (10(-7) M)-, and KCl (50 mM)-induced constrictions were followed by potent dilations. Inhibition of NO synthase with N(omega)-nitro-L-arginine (L-NNA, 2 x 10(-4) 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 (P(e)) to 75 mmHg for 20 s and 1 and 2 min decreased vessel diameter. After release of P(e), arterioles dilated as a function of the duration of diameter reduction by P(e). Removal of the endothelium or administration of L-NNA significantly diminished the post-P(e) 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.
authors.affiliation: Department of Physiology, New York Medical College, Valhalla, New York 10595, USA.
authors.forename: D
authors.initials: D
authors.lastname: Sun
authors.forename: A
authors.initials: A
authors.lastname: Huang
authors.forename: F A
authors.initials: FA
authors.lastname: Recchia
authors.forename: Y
authors.initials: Y
authors.lastname: Cui
authors.forename: E J
authors.initials: EJ
authors.lastname: Messina
authors.forename: A
authors.initials: A
authors.lastname: Koller
authors.forename: G
authors.initials: G
authors.lastname: Kaley
mesh_terms: D019796:15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid / Q000494:pharmacology; D000818:Animals; D001160:Arterioles / Q000166:cytology / Q000502:physiology; D048429:Cell Size / Q000502:physiology; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000166:cytology* / Q000187:drug effects / Q000201:enzymology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D008297:Male; D008638:Mesenteric Arteries / Q000166:cytology / Q000502:physiology*; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism; D009573:Nitrites / Q000378:metabolism; D019335:Nitroarginine / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D011189:Potassium Chloride / Q000494:pharmacology; D011312:Pressure; D051381:Rats; D017208:Rats, Wistar; D013314:Stress, Mechanical; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014664:Vasodilation / Q000502:physiology*
chemical_list: D004791:Enzyme Inhibitors; D009573:Nitrites; D014662:Vasoconstrictor Agents; D010656:Phenylephrine; D019335:Nitroarginine; D009569:Nitric Oxide; D011189:Potassium Chloride; D019796:15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid; D019001:Nitric Oxide Synthase