The aim was to examine the influence of the endothelium on acetylcholine (ACh) and vasoactive intestinal polypeptide (VIP) functional responses in the isolated glandular branch of rabbit facial artery precontracted with phenylephrine as well as the potential contribution of nitric oxide (NO) and prostanoids in the ACh- and VIP-induced effects. Acetylcholine caused endothelium-dependent and VIP endothelium-independent relaxations of facial artery. The effect of ACh was partly inhibited by NG-monomethyl-l-arginine (l-NMMA, a non-selective NO synthase inhibitor) or by indomethacin (a cyclooxygenase inhibitor) while being completely blocked after concomitant addition of l-NMMA and indomethacin. The relaxation of the facial artery caused by ACh was unaffected by 65 mm KCl. The VIP-induced vasodilation was potentiated by forskolin (an adenylate cyclase stimulator) and partly reduced by l-NMMA or S-methyl-l-thiocitrulline (l-SMTC, a neuronal NO synthase inhibitor), whereas it was unaffected b...y indomethacin. These results suggest that ACh effects on the rabbit facial artery are mediated through release of endothelium-derived NO and cyclooxygenase products, while the effect of VIP is most probably mediated by an increase of cyclic adenosine 3',5'-monophosphate (cAMP) in vascular smooth muscles and by VIP-induced release of NO from perivascular nerve fibers.
TY - JOUR
AU - Stojić, Dragica
AU - Radenković, Miroslav
AU - Kršljak, Elena
AU - Popović, Jelena
AU - Pešić, Srđan
AU - Grbović, Leposava
PY - 2003
UR - https://smile.stomf.bg.ac.rs/handle/123456789/2590
AB - The aim was to examine the influence of the endothelium on acetylcholine (ACh) and vasoactive intestinal polypeptide (VIP) functional responses in the isolated glandular branch of rabbit facial artery precontracted with phenylephrine as well as the potential contribution of nitric oxide (NO) and prostanoids in the ACh- and VIP-induced effects. Acetylcholine caused endothelium-dependent and VIP endothelium-independent relaxations of facial artery. The effect of ACh was partly inhibited by NG-monomethyl-l-arginine (l-NMMA, a non-selective NO synthase inhibitor) or by indomethacin (a cyclooxygenase inhibitor) while being completely blocked after concomitant addition of l-NMMA and indomethacin. The relaxation of the facial artery caused by ACh was unaffected by 65 mm KCl. The VIP-induced vasodilation was potentiated by forskolin (an adenylate cyclase stimulator) and partly reduced by l-NMMA or S-methyl-l-thiocitrulline (l-SMTC, a neuronal NO synthase inhibitor), whereas it was unaffected by indomethacin. These results suggest that ACh effects on the rabbit facial artery are mediated through release of endothelium-derived NO and cyclooxygenase products, while the effect of VIP is most probably mediated by an increase of cyclic adenosine 3',5'-monophosphate (cAMP) in vascular smooth muscles and by VIP-induced release of NO from perivascular nerve fibers.
PB - John Wiley & Sons, Inc.
T2 - European Journal of Oral Sciences
T1 - Influence of the endothelium on the vasorelaxant response to acetylcholine and vasoactive intestinal polypeptide in the isolated rabbit facial artery
VL - 111
IS - 2
SP - 137
EP - 143
DO - 10.1034/j.1600-0722.2003.00021.x
ER -
@article{
author = "Stojić, Dragica and Radenković, Miroslav and Kršljak, Elena and Popović, Jelena and Pešić, Srđan and Grbović, Leposava",
year = "2003",
abstract = "The aim was to examine the influence of the endothelium on acetylcholine (ACh) and vasoactive intestinal polypeptide (VIP) functional responses in the isolated glandular branch of rabbit facial artery precontracted with phenylephrine as well as the potential contribution of nitric oxide (NO) and prostanoids in the ACh- and VIP-induced effects. Acetylcholine caused endothelium-dependent and VIP endothelium-independent relaxations of facial artery. The effect of ACh was partly inhibited by NG-monomethyl-l-arginine (l-NMMA, a non-selective NO synthase inhibitor) or by indomethacin (a cyclooxygenase inhibitor) while being completely blocked after concomitant addition of l-NMMA and indomethacin. The relaxation of the facial artery caused by ACh was unaffected by 65 mm KCl. The VIP-induced vasodilation was potentiated by forskolin (an adenylate cyclase stimulator) and partly reduced by l-NMMA or S-methyl-l-thiocitrulline (l-SMTC, a neuronal NO synthase inhibitor), whereas it was unaffected by indomethacin. These results suggest that ACh effects on the rabbit facial artery are mediated through release of endothelium-derived NO and cyclooxygenase products, while the effect of VIP is most probably mediated by an increase of cyclic adenosine 3',5'-monophosphate (cAMP) in vascular smooth muscles and by VIP-induced release of NO from perivascular nerve fibers.",
publisher = "John Wiley & Sons, Inc.",
journal = "European Journal of Oral Sciences",
title = "Influence of the endothelium on the vasorelaxant response to acetylcholine and vasoactive intestinal polypeptide in the isolated rabbit facial artery",
volume = "111",
number = "2",
pages = "137-143",
doi = "10.1034/j.1600-0722.2003.00021.x"
}
Stojić, D., Radenković, M., Kršljak, E., Popović, J., Pešić, S.,& Grbović, L.. (2003). Influence of the endothelium on the vasorelaxant response to acetylcholine and vasoactive intestinal polypeptide in the isolated rabbit facial artery. in European Journal of Oral Sciences
John Wiley & Sons, Inc.., 111(2), 137-143.
https://doi.org/10.1034/j.1600-0722.2003.00021.x
Stojić D, Radenković M, Kršljak E, Popović J, Pešić S, Grbović L. Influence of the endothelium on the vasorelaxant response to acetylcholine and vasoactive intestinal polypeptide in the isolated rabbit facial artery. in European Journal of Oral Sciences. 2003;111(2):137-143.
doi:10.1034/j.1600-0722.2003.00021.x .
Stojić, Dragica, Radenković, Miroslav, Kršljak, Elena, Popović, Jelena, Pešić, Srđan, Grbović, Leposava, "Influence of the endothelium on the vasorelaxant response to acetylcholine and vasoactive intestinal polypeptide in the isolated rabbit facial artery" in European Journal of Oral Sciences, 111, no. 2 (2003):137-143,
https://doi.org/10.1034/j.1600-0722.2003.00021.x . .
, 
