title: Dietary silica modifies the characteristics of endothelial dilation in rat aorta.
abstract: Considering the importance of nitric oxide generation in the regulation of vessel tone, reduced endothelial nitric oxide synthase (eNOS) expression in alveolar macrophages exposed to short-term silica (Si) suggests the possibility of Si-induced changes in endothelial functions. In this experimental study, the functional changes of the endothelial cells were investigated in the aortic rings of rats subjected to 50 mg Si/kg body weight in their drinking water for 8 days. Norepinephrine elicited contractility and dilation response to acetylcholine (ACh) was significantly high in the aortic rings of Si-treated group. Alteration in receptor-independent endothelial response to A23187 in the aortic rings of Si-exposed rats was less obvious, but sodium nitroprusside (SNP)-elicited dilation was reduced significantly. A23187-induced relaxation was fully eliminated with N-nitro-L-arginine methyl ester (L-NAME) pretreatment, whereas 19.24 +/- 4.36% of ACh response was L-NAME resistant and eliminated with 10-5 M tetraethylammonium (TEA). Despite a significant reduction in the share of NO, the contribution of indomethacine (IND)-sensitive relaxation to ACh response remained unchanged in Si group. As a result, our findings demonstrated that Si both modifies the characteristics of endothelial relaxants and attenuates smooth muscle cell responsiveness to NO. Si-induced reduced NO association with elevated endothelium-derived hyperpolarizing factor (EDHF) in response to ACh, together with reduced NO sensitization, might have clinical importance in cardiovascular pathology.
authors.affiliation: Department of Physiology, Medical Faculty, Akdeniz University, Antalya, Turkey. onerg@akdeniz.edu.tr
authors.forename: Gülsen
authors.initials: G
authors.lastname: Oner
authors.forename: Selma
authors.initials: S
authors.lastname: Cirrik
authors.forename: Mehmet
authors.initials: M
authors.lastname: Bulbul
authors.forename: Selahattin
authors.initials: S
authors.lastname: Yuksel
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D001011:Aorta / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D001685:Biological Factors / Q000378:metabolism; D019587:Dietary Supplements; D004347:Drug Interactions; D042783:Endothelial Cells / Q000187:drug effects* / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005526:Food, Formulated; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism*; D020030:Nitric Oxide Donors / Q000494:pharmacology; D009924:Organ Culture Techniques; D026902:Potassium Channel Blockers / Q000494:pharmacology; D051381:Rats; D012822:Silicon Dioxide / Q000008:administration & dosage / Q000494:pharmacology*; D019789:Tetraethylammonium / Q000494:pharmacology; D013995:Time; D015854:Up-Regulation / Q000187:drug effects / Q000502:physiology; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014664:Vasodilation / Q000187:drug effects* / Q000502:physiology; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D001685:Biological Factors; D004791:Enzyme Inhibitors; D020030:Nitric Oxide Donors; D026902:Potassium Channel Blockers; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; C067410:endothelium-dependent hyperpolarization factor; D009569:Nitric Oxide; D019789:Tetraethylammonium; D012822:Silicon Dioxide; D019331:NG-Nitroarginine Methyl Ester