University of Hertfordshire

Contribution of COX-1 products to contractions of the mouse aorta and bronchus.

Research output: Contribution to conferenceAbstract

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Contribution of COX-1 products to contractions of the mouse aorta and bronchus. / Harrington, Louise; Reed, Anne; Warner, Tim; Mitchell, Jane A.

2007. Abstract from BPS Winter Meeting, London, United Kingdom.

Research output: Contribution to conferenceAbstract

Harvard

Harrington, L, Reed, A, Warner, T & Mitchell, JA 2007, 'Contribution of COX-1 products to contractions of the mouse aorta and bronchus.' BPS Winter Meeting, London, United Kingdom, 15/12/10 - 17/12/10, .

APA

Harrington, L., Reed, A., Warner, T., & Mitchell, J. A. (2007). Contribution of COX-1 products to contractions of the mouse aorta and bronchus.. Abstract from BPS Winter Meeting, London, United Kingdom.

Vancouver

Harrington L, Reed A, Warner T, Mitchell JA. Contribution of COX-1 products to contractions of the mouse aorta and bronchus.. 2007. Abstract from BPS Winter Meeting, London, United Kingdom.

Author

Harrington, Louise ; Reed, Anne ; Warner, Tim ; Mitchell, Jane A. / Contribution of COX-1 products to contractions of the mouse aorta and bronchus. Abstract from BPS Winter Meeting, London, United Kingdom.

Bibtex

@conference{e4307923e99244d8bcaef8672cb0b1da,
title = "Contribution of COX-1 products to contractions of the mouse aorta and bronchus.",
abstract = "Cyclooxygenase (COX) mediates the production of prostaglandin (PG)H2, the precursor to down-stream prostanoids, from arachidonic acid. COX exists in two isoforms; constitutively expressed COX-1, and inducible COX-2. In the mouse bronchus, COX-1 derived dilator prostanoids predominate whereas in mouse aorta, COX-1 derived constrictor prostanoids predominate (C023, this meeting). Here we have investigated the effect of NSAIDs and COX-2 selective drugs on contraction of vessels (aorta) and airway (bronchi) of the mouse. Male COX-1-/- mice or C57Bl6 wild type mice (25-30g) were killed by cervical dislocation, and rings of aorta and bronchus were mounted in isometric wire myographs. Tissues were incubated with: COX-2 selective drugs, 10-5M lumiracoxib, 10-5M parecoxib, and NSAIDs, 10-4M naproxen, 10-5M ibuprofen, or 5l DMSO (vehicle control). Contractions of aortae induced by U46619 (10-9 to 3x10-7M), phenylephrine (PE; 10-9 to 10-5M) were recorded and expressed as kPa by taking account of the vessel diameters. Contractions of bronchi to U46619 (10-8 to 3x10-6M) and acetylcholine (Ach; 10-8 to 3x10-4M) were recorded, and expressed as {\%} of the maximum response to KCl (0.124M). Figure 1. Concentration response curve to U46619 in (A.) wild type and (B.) COX-1-/- aortae. Tissues were incubated in the presence of 10-5M lumiracoxib for 30 minutes. Data shown is mean ± SEM, n=4-6; * p<0.05 by two way ANOVA.Lumiracoxib (Fig.1A), parecoxib, naproxen and ibuprofen inhibited contraction induced by the thromboxane mimetic U46619 in wild type mouse aorta, but not in COX-1-/- aorta (Fig.1B). Incubation with all COX inhibitor drugs increased U46619 contraction in wild type bronchi, and not COX-1-/- mice. These observations indicate that COX-2 selective drugs lumiracoxib and parecoxib have inhibitory effects on COX-1 activity. This is consistent with the evidence that COX-2 selective drugs have cardiovascular side effects.This work was funded by the Wellcome Trust. COX-1-/- mice were provided by Prof A. Ahluwalia and Dr. R. Scotland",
author = "Louise Harrington and Anne Reed and Tim Warner and Mitchell, {Jane A.}",
year = "2007",
month = "12",
language = "English",
note = "BPS Winter Meeting ; Conference date: 15-12-2010 Through 17-12-2010",

}

RIS

TY - CONF

T1 - Contribution of COX-1 products to contractions of the mouse aorta and bronchus.

AU - Harrington, Louise

AU - Reed, Anne

AU - Warner, Tim

AU - Mitchell, Jane A.

PY - 2007/12

Y1 - 2007/12

N2 - Cyclooxygenase (COX) mediates the production of prostaglandin (PG)H2, the precursor to down-stream prostanoids, from arachidonic acid. COX exists in two isoforms; constitutively expressed COX-1, and inducible COX-2. In the mouse bronchus, COX-1 derived dilator prostanoids predominate whereas in mouse aorta, COX-1 derived constrictor prostanoids predominate (C023, this meeting). Here we have investigated the effect of NSAIDs and COX-2 selective drugs on contraction of vessels (aorta) and airway (bronchi) of the mouse. Male COX-1-/- mice or C57Bl6 wild type mice (25-30g) were killed by cervical dislocation, and rings of aorta and bronchus were mounted in isometric wire myographs. Tissues were incubated with: COX-2 selective drugs, 10-5M lumiracoxib, 10-5M parecoxib, and NSAIDs, 10-4M naproxen, 10-5M ibuprofen, or 5l DMSO (vehicle control). Contractions of aortae induced by U46619 (10-9 to 3x10-7M), phenylephrine (PE; 10-9 to 10-5M) were recorded and expressed as kPa by taking account of the vessel diameters. Contractions of bronchi to U46619 (10-8 to 3x10-6M) and acetylcholine (Ach; 10-8 to 3x10-4M) were recorded, and expressed as % of the maximum response to KCl (0.124M). Figure 1. Concentration response curve to U46619 in (A.) wild type and (B.) COX-1-/- aortae. Tissues were incubated in the presence of 10-5M lumiracoxib for 30 minutes. Data shown is mean ± SEM, n=4-6; * p<0.05 by two way ANOVA.Lumiracoxib (Fig.1A), parecoxib, naproxen and ibuprofen inhibited contraction induced by the thromboxane mimetic U46619 in wild type mouse aorta, but not in COX-1-/- aorta (Fig.1B). Incubation with all COX inhibitor drugs increased U46619 contraction in wild type bronchi, and not COX-1-/- mice. These observations indicate that COX-2 selective drugs lumiracoxib and parecoxib have inhibitory effects on COX-1 activity. This is consistent with the evidence that COX-2 selective drugs have cardiovascular side effects.This work was funded by the Wellcome Trust. COX-1-/- mice were provided by Prof A. Ahluwalia and Dr. R. Scotland

AB - Cyclooxygenase (COX) mediates the production of prostaglandin (PG)H2, the precursor to down-stream prostanoids, from arachidonic acid. COX exists in two isoforms; constitutively expressed COX-1, and inducible COX-2. In the mouse bronchus, COX-1 derived dilator prostanoids predominate whereas in mouse aorta, COX-1 derived constrictor prostanoids predominate (C023, this meeting). Here we have investigated the effect of NSAIDs and COX-2 selective drugs on contraction of vessels (aorta) and airway (bronchi) of the mouse. Male COX-1-/- mice or C57Bl6 wild type mice (25-30g) were killed by cervical dislocation, and rings of aorta and bronchus were mounted in isometric wire myographs. Tissues were incubated with: COX-2 selective drugs, 10-5M lumiracoxib, 10-5M parecoxib, and NSAIDs, 10-4M naproxen, 10-5M ibuprofen, or 5l DMSO (vehicle control). Contractions of aortae induced by U46619 (10-9 to 3x10-7M), phenylephrine (PE; 10-9 to 10-5M) were recorded and expressed as kPa by taking account of the vessel diameters. Contractions of bronchi to U46619 (10-8 to 3x10-6M) and acetylcholine (Ach; 10-8 to 3x10-4M) were recorded, and expressed as % of the maximum response to KCl (0.124M). Figure 1. Concentration response curve to U46619 in (A.) wild type and (B.) COX-1-/- aortae. Tissues were incubated in the presence of 10-5M lumiracoxib for 30 minutes. Data shown is mean ± SEM, n=4-6; * p<0.05 by two way ANOVA.Lumiracoxib (Fig.1A), parecoxib, naproxen and ibuprofen inhibited contraction induced by the thromboxane mimetic U46619 in wild type mouse aorta, but not in COX-1-/- aorta (Fig.1B). Incubation with all COX inhibitor drugs increased U46619 contraction in wild type bronchi, and not COX-1-/- mice. These observations indicate that COX-2 selective drugs lumiracoxib and parecoxib have inhibitory effects on COX-1 activity. This is consistent with the evidence that COX-2 selective drugs have cardiovascular side effects.This work was funded by the Wellcome Trust. COX-1-/- mice were provided by Prof A. Ahluwalia and Dr. R. Scotland

M3 - Abstract

ER -