Extraendothelial and constitutive COX-2 expression is involved in the contractile effect of angiotensin II in the rat aorta

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Abstract

1 The role of the extraendothelial and constitutive isoforms of cyclo-oxygenase-2 (COX-2) in the contractile effect of angiotensin II (Ang II) was investigated using thoracic and abdominal aortic rings without endothelium from young Wistar rats. 2 Ang II elicited similar contractions in both aortic segments, and the effect was inhibited by pretreatment with NS398 (a selective COX-2 inhibitor) but not SC-560 [selective cyclo-oxygenase-1 (COX-1) inhibitor]. 3 COX-2 mRNA was expressed under basal conditions in both aortic segments. Additionally, Ang II increased COX-2 mRNA expression in the abdominal but not the thoracic segment, while cycloheximide (a protein synthesis inhibitor) did not affect the contractile response to Ang II in either of the two segments; this suggests that the effect is not associated with de novo COX-2 synthesis. 4 In conclusion, the basal amount of COX-2 found in aortic smooth muscle cells is sufficient to explain the production of the prostanoids related to the contractile effect of Ang II. The production of these prostanoids, which are derived from constitutive COX-2, occurs independently of the endothelium vascular system. © 2010 Blackwell Publishing Ltd.
Original languageAmerican English
Pages (from-to)205-211
Number of pages183
JournalAutonomic and Autacoid Pharmacology
DOIs
StatePublished - 1 Oct 2010

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Prostaglandin-Endoperoxide Synthases
Angiotensin II
Aorta
Cyclooxygenase Inhibitors
Prostaglandins
Thorax
Messenger RNA
Protein Synthesis Inhibitors
Vascular Endothelium
Cycloheximide
Smooth Muscle Myocytes
Endothelium
Wistar Rats
Protein Isoforms

Cite this

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title = "Extraendothelial and constitutive COX-2 expression is involved in the contractile effect of angiotensin II in the rat aorta",
abstract = "1 The role of the extraendothelial and constitutive isoforms of cyclo-oxygenase-2 (COX-2) in the contractile effect of angiotensin II (Ang II) was investigated using thoracic and abdominal aortic rings without endothelium from young Wistar rats. 2 Ang II elicited similar contractions in both aortic segments, and the effect was inhibited by pretreatment with NS398 (a selective COX-2 inhibitor) but not SC-560 [selective cyclo-oxygenase-1 (COX-1) inhibitor]. 3 COX-2 mRNA was expressed under basal conditions in both aortic segments. Additionally, Ang II increased COX-2 mRNA expression in the abdominal but not the thoracic segment, while cycloheximide (a protein synthesis inhibitor) did not affect the contractile response to Ang II in either of the two segments; this suggests that the effect is not associated with de novo COX-2 synthesis. 4 In conclusion, the basal amount of COX-2 found in aortic smooth muscle cells is sufficient to explain the production of the prostanoids related to the contractile effect of Ang II. The production of these prostanoids, which are derived from constitutive COX-2, occurs independently of the endothelium vascular system. {\circledC} 2010 Blackwell Publishing Ltd.",
author = "Castillo-Hern{\'a}ndez, {M. C.} and Martinez-Godinez, {M. A.} and G. Guevara-Balcazar and A. Miliar-Garcia and J. Mancilla and Lopez-Mayorga, {R. M.} and Castillo-Henkel, {E. F.} and C. Castillo-Henkel",
year = "2010",
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doi = "10.1111/j.1474-8673.2010.00457.x",
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T1 - Extraendothelial and constitutive COX-2 expression is involved in the contractile effect of angiotensin II in the rat aorta

AU - Castillo-Hernández, M. C.

AU - Martinez-Godinez, M. A.

AU - Guevara-Balcazar, G.

AU - Miliar-Garcia, A.

AU - Mancilla, J.

AU - Lopez-Mayorga, R. M.

AU - Castillo-Henkel, E. F.

AU - Castillo-Henkel, C.

PY - 2010/10/1

Y1 - 2010/10/1

N2 - 1 The role of the extraendothelial and constitutive isoforms of cyclo-oxygenase-2 (COX-2) in the contractile effect of angiotensin II (Ang II) was investigated using thoracic and abdominal aortic rings without endothelium from young Wistar rats. 2 Ang II elicited similar contractions in both aortic segments, and the effect was inhibited by pretreatment with NS398 (a selective COX-2 inhibitor) but not SC-560 [selective cyclo-oxygenase-1 (COX-1) inhibitor]. 3 COX-2 mRNA was expressed under basal conditions in both aortic segments. Additionally, Ang II increased COX-2 mRNA expression in the abdominal but not the thoracic segment, while cycloheximide (a protein synthesis inhibitor) did not affect the contractile response to Ang II in either of the two segments; this suggests that the effect is not associated with de novo COX-2 synthesis. 4 In conclusion, the basal amount of COX-2 found in aortic smooth muscle cells is sufficient to explain the production of the prostanoids related to the contractile effect of Ang II. The production of these prostanoids, which are derived from constitutive COX-2, occurs independently of the endothelium vascular system. © 2010 Blackwell Publishing Ltd.

AB - 1 The role of the extraendothelial and constitutive isoforms of cyclo-oxygenase-2 (COX-2) in the contractile effect of angiotensin II (Ang II) was investigated using thoracic and abdominal aortic rings without endothelium from young Wistar rats. 2 Ang II elicited similar contractions in both aortic segments, and the effect was inhibited by pretreatment with NS398 (a selective COX-2 inhibitor) but not SC-560 [selective cyclo-oxygenase-1 (COX-1) inhibitor]. 3 COX-2 mRNA was expressed under basal conditions in both aortic segments. Additionally, Ang II increased COX-2 mRNA expression in the abdominal but not the thoracic segment, while cycloheximide (a protein synthesis inhibitor) did not affect the contractile response to Ang II in either of the two segments; this suggests that the effect is not associated with de novo COX-2 synthesis. 4 In conclusion, the basal amount of COX-2 found in aortic smooth muscle cells is sufficient to explain the production of the prostanoids related to the contractile effect of Ang II. The production of these prostanoids, which are derived from constitutive COX-2, occurs independently of the endothelium vascular system. © 2010 Blackwell Publishing Ltd.

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