title: Effect of engineered nanoparticles on vasomotor responses in rat intrapulmonary artery.
abstract: Pulmonary circulation could be one of the primary vascular targets of finest particles that can deeply penetrate into the lungs after inhalation. We investigated the effects of engineered nanoparticles on vasomotor responses of small intrapulmonary arteries using isometric tension measurements. Acute in vitro exposure to carbon nanoparticles (CNP) decreased, and in some case abolished, the vasomotor responses induced by several vasoactive agents, whereas acute exposure to titanium dioxide nanoparticles (TiO(2)NP) did not. This could be attributed to a decrease in the activity of those vasoactive agents (including PGF(2)(alpha), serotonin, endothelin-1 and acetylcholine), as suggested when they were exposed to CNP before being applied to arteries. Also, CNP decreased the contraction induced by 30 mM KCl, without decreasing its activity. After endoplasmic reticulum calcium stores depletion (by caffeine and thapsigargin), CaCl(2) addition induced a contraction, dependent on Store-Operated Calcium Channels that was not modified by acute CNP exposure. Further addition of 30 mM KCl elicited a contraction, originating from activation of Voltage-Operated Calcium Channels that was diminished by CNP. Contractile responses to PGF(2)(alpha) or KCl, and relaxation to acetylcholine were modified neither in pulmonary arteries exposed in vitro for prolonged time to CNP or TiO(2)NP, nor in those removed from rats intratracheally instilled with CNP or TiO(2)NP. In conclusion, prolonged in vitro or in vivo exposure to CNP or TiO(2)NP does not affect vasomotor responses of pulmonary arteries. However, acute exposure to CNP decreases contraction mediated by activation of Voltage-Operated, but not Store-Operated, Calcium Channels. Moreover, interaction of some vasoactive agents with CNP decreases their biological activity that might lead to misinterpretation of experimental data.
authors.affiliation: Université Bordeaux 2, Bordeaux, F-33076, France. arnaud.courtois@u-bordeaux2.fr
authors.forename: Arnaud
authors.initials: A
authors.lastname: Courtois
authors.forename: Pascal
authors.initials: P
authors.lastname: Andujar
authors.forename: Yannick
authors.initials: Y
authors.lastname: Ladeiro
authors.forename: Thomas
authors.initials: T
authors.lastname: Ducret
authors.forename: Françoise
authors.initials: F
authors.lastname: Rogerieux
authors.forename: Ghislaine
authors.initials: G
authors.lastname: Lacroix
authors.forename: Isabelle
authors.initials: I
authors.lastname: Baudrimont
authors.forename: Christelle
authors.initials: C
authors.lastname: Guibert
authors.forename: Etienne
authors.initials: E
authors.lastname: Roux
authors.forename: Mireille
authors.initials: M
authors.lastname: Canal-Raffin
authors.forename: Patrick
authors.initials: P
authors.lastname: Brochard
authors.forename: Francelyne
authors.initials: F
authors.lastname: Marano
authors.forename: Roger
authors.initials: R
authors.lastname: Marthan
authors.forename: Bernard
authors.initials: B
authors.lastname: Muller
mesh_terms: D000818:Animals; D015220:Calcium Channels / Q000502:physiology; D002244:Carbon / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D004721:Endoplasmic Reticulum / Q000378:metabolism; D019570:Inhalation Exposure / Q000009:adverse effects; D007537:Isometric Contraction / Q000187:drug effects*; D008297:Male; D053758:Nanoparticles; D011651:Pulmonary Artery / Q000187:drug effects* / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D017208:Rats, Wistar; D014025:Titanium / Q000494:pharmacology*; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D015220:Calcium Channels; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; C009495:titanium dioxide; D002244:Carbon; D014025:Titanium