Vasorelaxant effects of Clearfil SE Bond and Clearfil S(3) Bond mediated by calcium antagonistic action.
Dental adhesives can alter the contractility of vascular tissue via different mechanisms. The aim of this study was to investigate and compare the vascular action of two self-etch adhesive systems, Clearfil SE Bond (CSEB) and Clearfil S(3) Bond (CS3B). Responses of isolated rat thoracic aorta rings were recorded isometrically by force displacement transducers. Following pre-contraction of aorta rings, relaxations to the independent and mixed components of CSEB and CS3B were recorded in the absence and presence of nitric oxide synthase (NOS) inhibitor (N(omega)-nitro-L-arginine methyl ester (N-LAME)), cyclooxygenase (COX) inhibitor (indomethacin) and K+ channel inhibitors (tetraethylammonium, glibenclamide and 4-aminopyridine). We also tested the effects of CSEB and CS3B in endothelium-intact and -denuded rat thoracic aorta rings. To investigate the Ca2+-channel antagonistic effect of adhesive components, concentration-response curves to CaCl2 were obtained in the absence and presence of the components. The primer, the bond, and the mixture of CSEB and CS3B elicited concentration-dependent relaxations. Mechanical rubbing of the endothelium did not significantly modify the extent of vasorelaxation induced by the test materials. The vasorelaxant effect was mediated neither by NOS and COX inhibition nor by the tested K+ channel antagonists. Mechanical removal of the endothelium did not alter the vasodilatory effect induced by the self-etch adhesives. Both CSEB and CS3B significantly inhibited the contractions induced by CaCl2. These results demonstrate the vasodilatory effect induced by the self-etch adhesive systems through a Ca2+-antagonistic effect.
Seyrek
Melik
M
Department of Medical Pharmacology, Gulhane School of Medicine, Ankara, Turkey.
Guven
Gunseli
G
Vural
Ismail Mert
IM
Kaya
Ertugrul
E
Cehreli
Zafer C
ZC
Altun
Ceyhan
C
Yildiz
Oguzhan
O
D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000502:physiology; D002118:Calcium / Q000037:antagonists & inhibitors* / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000737:chemistry / Q000494:pharmacology*; D015220:Calcium Channels / Q000378:metabolism; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D003738:Dental Cements / Q000737:chemistry / Q000494:pharmacology*; D017220:Dentin-Bonding Agents / Q000737:chemistry / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D026902:Potassium Channel Blockers / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D019279:Resin Cements / Q000737:chemistry / Q000494:pharmacology*; D014664:Vasodilation / Q000187:drug effects*; D014665:Vasodilator Agents / Q000737:chemistry / Q000494:pharmacology*
D002121:Calcium Channel Blockers; D015220:Calcium Channels; C505694:Clearfil S3 Bond; C438313:Clearfil SE Bond; D016861:Cyclooxygenase Inhibitors; D003738:Dental Cements; D017220:Dentin-Bonding Agents; D026902:Potassium Channel Blockers; D019279:Resin Cements; D014665:Vasodilator Agents; D019001:Nitric Oxide Synthase; D002118:Calcium; D019331:NG-Nitroarginine Methyl Ester; D007213:Indomethacin