Des-Arg9-bradykinin causes kinin B1 receptor mediated endothelium-independent contractions in endotoxin-treated porcine coronary arteries

Amar S. More, Hye Min Kim, Gilson Khang, Tobias Hildebrandt, Christian Bernlöhr, Henri Doods, Paul M. Vanhoutte, Dongmei Wu

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

This study examined responses of isolated pig coronary arteries after kinin B1 receptor induction by endotoxin. Des-Arg9-bradykinin (DBK) induced concentration-dependent, endothelium-independent contractions in lipopolysaccharide (LPS)-treated but not untreated arterial rings. The B1-receptor antagonist SSR240612, but not the B2-receptor antagonist HOE140, prevented the endothelium-independent contractions to DBK. The DBK-induced contractions were blocked by indomethacin (nonselective cyclooxygenase [COX] inhibitor), celecoxib (selective COX-2 inhibitor), and terbogrel (thromboxane-prostanoid [TP] receptor antagonist) but not valeryl salicylate (selective COX-1 inhibitor), AH6809 (an E prostanoid [EP] and PGD2 receptor [DP1] receptor antagonist), AL 8810 (a selective PGF [FP] receptor antagonist), or RO1138452 (a selective I prostanoid [IP] receptor antagonist). They were attenuated by N-(p-amylcinnamoyl) anthranilic acid (ACA), and by DETCA plus tiron but not by l-NAME. Quantitative RT-PCR revealed excessive up-regulations of mRNA expressions of B1 receptors, COX-2, and thromboxane A synthase 1 (TBXAS1) following LPS incubation, but not of B2 receptors or COX-1. The present data demonstrate that B1 receptors are coupled to COX-2 in causing endothelium-independent contractions in endotoxin-treated pig coronary arteries. Accordingly, kinin B1 receptor induction during inflammation may have a pathological significance in the vasculature, particular in coronary arteries with dysfunctional endothelial cells.

Original languageEnglish (US)
Pages (from-to)18-24
Number of pages7
JournalPharmacological Research
Volume90
DOIs
StatePublished - 2014
Externally publishedYes

Fingerprint

Kinins
Bradykinin
Endotoxins
Prostaglandins
Endothelium
Coronary Vessels
Cyclooxygenase 1
Swine
Cyclooxygenase Inhibitors
Celecoxib
Cyclooxygenase 2
Lipopolysaccharides
1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt
Thromboxane-A Synthase
Thromboxane Receptors
Dinoprost
Salicylates
Cyclooxygenase 2 Inhibitors
Indomethacin
Up-Regulation

Keywords

  • Cyclooxygenase-2
  • Kinin B1 receptor
  • Vascular contraction
  • Vascular inflammation

ASJC Scopus subject areas

  • Pharmacology
  • Medicine(all)

Cite this

Des-Arg9-bradykinin causes kinin B1 receptor mediated endothelium-independent contractions in endotoxin-treated porcine coronary arteries. / More, Amar S.; Kim, Hye Min; Khang, Gilson; Hildebrandt, Tobias; Bernlöhr, Christian; Doods, Henri; Vanhoutte, Paul M.; Wu, Dongmei.

In: Pharmacological Research, Vol. 90, 2014, p. 18-24.

Research output: Contribution to journalArticle

More, Amar S. ; Kim, Hye Min ; Khang, Gilson ; Hildebrandt, Tobias ; Bernlöhr, Christian ; Doods, Henri ; Vanhoutte, Paul M. ; Wu, Dongmei. / Des-Arg9-bradykinin causes kinin B1 receptor mediated endothelium-independent contractions in endotoxin-treated porcine coronary arteries. In: Pharmacological Research. 2014 ; Vol. 90. pp. 18-24.
@article{f33280298fb44fc8bf34aa7b7ebd5fe7,
title = "Des-Arg9-bradykinin causes kinin B1 receptor mediated endothelium-independent contractions in endotoxin-treated porcine coronary arteries",
abstract = "This study examined responses of isolated pig coronary arteries after kinin B1 receptor induction by endotoxin. Des-Arg9-bradykinin (DBK) induced concentration-dependent, endothelium-independent contractions in lipopolysaccharide (LPS)-treated but not untreated arterial rings. The B1-receptor antagonist SSR240612, but not the B2-receptor antagonist HOE140, prevented the endothelium-independent contractions to DBK. The DBK-induced contractions were blocked by indomethacin (nonselective cyclooxygenase [COX] inhibitor), celecoxib (selective COX-2 inhibitor), and terbogrel (thromboxane-prostanoid [TP] receptor antagonist) but not valeryl salicylate (selective COX-1 inhibitor), AH6809 (an E prostanoid [EP] and PGD2 receptor [DP1] receptor antagonist), AL 8810 (a selective PGF2α [FP] receptor antagonist), or RO1138452 (a selective I prostanoid [IP] receptor antagonist). They were attenuated by N-(p-amylcinnamoyl) anthranilic acid (ACA), and by DETCA plus tiron but not by l-NAME. Quantitative RT-PCR revealed excessive up-regulations of mRNA expressions of B1 receptors, COX-2, and thromboxane A synthase 1 (TBXAS1) following LPS incubation, but not of B2 receptors or COX-1. The present data demonstrate that B1 receptors are coupled to COX-2 in causing endothelium-independent contractions in endotoxin-treated pig coronary arteries. Accordingly, kinin B1 receptor induction during inflammation may have a pathological significance in the vasculature, particular in coronary arteries with dysfunctional endothelial cells.",
keywords = "Cyclooxygenase-2, Kinin B1 receptor, Vascular contraction, Vascular inflammation",
author = "More, {Amar S.} and Kim, {Hye Min} and Gilson Khang and Tobias Hildebrandt and Christian Bernl{\"o}hr and Henri Doods and Vanhoutte, {Paul M.} and Dongmei Wu",
year = "2014",
doi = "10.1016/j.phrs.2014.09.001",
language = "English (US)",
volume = "90",
pages = "18--24",
journal = "Pharmacological Research",
issn = "1043-6618",
publisher = "Academic Press Inc.",

}

TY - JOUR

T1 - Des-Arg9-bradykinin causes kinin B1 receptor mediated endothelium-independent contractions in endotoxin-treated porcine coronary arteries

AU - More, Amar S.

AU - Kim, Hye Min

AU - Khang, Gilson

AU - Hildebrandt, Tobias

AU - Bernlöhr, Christian

AU - Doods, Henri

AU - Vanhoutte, Paul M.

AU - Wu, Dongmei

PY - 2014

Y1 - 2014

N2 - This study examined responses of isolated pig coronary arteries after kinin B1 receptor induction by endotoxin. Des-Arg9-bradykinin (DBK) induced concentration-dependent, endothelium-independent contractions in lipopolysaccharide (LPS)-treated but not untreated arterial rings. The B1-receptor antagonist SSR240612, but not the B2-receptor antagonist HOE140, prevented the endothelium-independent contractions to DBK. The DBK-induced contractions were blocked by indomethacin (nonselective cyclooxygenase [COX] inhibitor), celecoxib (selective COX-2 inhibitor), and terbogrel (thromboxane-prostanoid [TP] receptor antagonist) but not valeryl salicylate (selective COX-1 inhibitor), AH6809 (an E prostanoid [EP] and PGD2 receptor [DP1] receptor antagonist), AL 8810 (a selective PGF2α [FP] receptor antagonist), or RO1138452 (a selective I prostanoid [IP] receptor antagonist). They were attenuated by N-(p-amylcinnamoyl) anthranilic acid (ACA), and by DETCA plus tiron but not by l-NAME. Quantitative RT-PCR revealed excessive up-regulations of mRNA expressions of B1 receptors, COX-2, and thromboxane A synthase 1 (TBXAS1) following LPS incubation, but not of B2 receptors or COX-1. The present data demonstrate that B1 receptors are coupled to COX-2 in causing endothelium-independent contractions in endotoxin-treated pig coronary arteries. Accordingly, kinin B1 receptor induction during inflammation may have a pathological significance in the vasculature, particular in coronary arteries with dysfunctional endothelial cells.

AB - This study examined responses of isolated pig coronary arteries after kinin B1 receptor induction by endotoxin. Des-Arg9-bradykinin (DBK) induced concentration-dependent, endothelium-independent contractions in lipopolysaccharide (LPS)-treated but not untreated arterial rings. The B1-receptor antagonist SSR240612, but not the B2-receptor antagonist HOE140, prevented the endothelium-independent contractions to DBK. The DBK-induced contractions were blocked by indomethacin (nonselective cyclooxygenase [COX] inhibitor), celecoxib (selective COX-2 inhibitor), and terbogrel (thromboxane-prostanoid [TP] receptor antagonist) but not valeryl salicylate (selective COX-1 inhibitor), AH6809 (an E prostanoid [EP] and PGD2 receptor [DP1] receptor antagonist), AL 8810 (a selective PGF2α [FP] receptor antagonist), or RO1138452 (a selective I prostanoid [IP] receptor antagonist). They were attenuated by N-(p-amylcinnamoyl) anthranilic acid (ACA), and by DETCA plus tiron but not by l-NAME. Quantitative RT-PCR revealed excessive up-regulations of mRNA expressions of B1 receptors, COX-2, and thromboxane A synthase 1 (TBXAS1) following LPS incubation, but not of B2 receptors or COX-1. The present data demonstrate that B1 receptors are coupled to COX-2 in causing endothelium-independent contractions in endotoxin-treated pig coronary arteries. Accordingly, kinin B1 receptor induction during inflammation may have a pathological significance in the vasculature, particular in coronary arteries with dysfunctional endothelial cells.

KW - Cyclooxygenase-2

KW - Kinin B1 receptor

KW - Vascular contraction

KW - Vascular inflammation

UR - http://www.scopus.com/inward/record.url?scp=84907702141&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84907702141&partnerID=8YFLogxK

U2 - 10.1016/j.phrs.2014.09.001

DO - 10.1016/j.phrs.2014.09.001

M3 - Article

VL - 90

SP - 18

EP - 24

JO - Pharmacological Research

JF - Pharmacological Research

SN - 1043-6618

ER -