Effects of hyperbaric oxygenation on vascular reactivity to angiotensin II and angiotensin-(1-7) in rats

Aleksandar Kibel, Ana Cavka, Anita Cosic, J R Falck, Ines Drenjancevic

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Objective: To assess and elucidate the mechanisms of hyperbaric oxygenation (HBO2) effects on vascular reactivity to angiotensin-(1-7) [ANG-(1-7)] and angiotensin II (ANG II). Methods: Rat aortic rings (HBO 2 vs. control group) were used to test responses to ANG II, ANG II+ ANG-(1-7) or ANG-(1-7) after noradrenaline precontraction in the presence/absence of MS-PPOH, a specific CYP 450-epoxygenase inhibitor, and glibenclamide, a KAT P channels inhibitor. mRNA expression studies of specific CYP isozymes have been conducted as well. Results: The mean contraction (expressed as percent of maximal contraction) for ANG II was similar between groups. Contraction for ANG II + ANG-(1-7) was 15% ± 10 (HBO2) and 20% ± 9 (control). There was a significant decrease between the contraction response to ANG II (HBO2) and the response to ANG II + ANG-(1-7) in the HBO2 group, without such a difference within the control group. Mean percentage of noradrenaline precontraction decrease after ANG-(1-7) addition was significantly different [10% ± 9 (control) and 19% ± 11 (HBO2)]. The epoxygenase inhibitor MS-PPOH in HBO2 animals reversed these changes. Glibenclamide had no effect on relaxation in response to ANG-(1-7). Expression of CYP4A2, CYP4A3 and CYP2J3 mRNA was not significantly altered with HBO, whereas CYP4A1 was significantly upregulated. Conclusions: Our results suggest a role for epoxyeicosatrienoic acids in modulating relaxation response to ANG-(1-7) with HBO2 that is conducted via potassium channels other than K AT P channels. HBO2 increased the responses to ANG-(1-7) after precontraction with noradrenaline. The difference between the response to ANG II in the HBO2 group and ANG II + ANG-(1-7) in the HBO 2 group (the contraction force of the peptide combination being lower), without such difference in the control group, suggests an influence of HBO2 on vascular reactivity.

Original languageEnglish (US)
Pages (from-to)1053-1066
Number of pages14
JournalUndersea and Hyperbaric Medicine
Volume39
Issue number6
StatePublished - Nov 2012

Fingerprint

Hyperbaric Oxygenation
Angiotensins
Blood Vessels
Angiotensin II
Norepinephrine
Glyburide
Control Groups
angiotensin I (1-7)
Messenger RNA
Potassium Channels
Isoenzymes

ASJC Scopus subject areas

  • Physiology (medical)
  • Pulmonary and Respiratory Medicine

Cite this

Effects of hyperbaric oxygenation on vascular reactivity to angiotensin II and angiotensin-(1-7) in rats. / Kibel, Aleksandar; Cavka, Ana; Cosic, Anita; Falck, J R; Drenjancevic, Ines.

In: Undersea and Hyperbaric Medicine, Vol. 39, No. 6, 11.2012, p. 1053-1066.

Research output: Contribution to journalArticle

Kibel, Aleksandar ; Cavka, Ana ; Cosic, Anita ; Falck, J R ; Drenjancevic, Ines. / Effects of hyperbaric oxygenation on vascular reactivity to angiotensin II and angiotensin-(1-7) in rats. In: Undersea and Hyperbaric Medicine. 2012 ; Vol. 39, No. 6. pp. 1053-1066.
@article{a3b30088e8c6462680baf785e9321f6b,
title = "Effects of hyperbaric oxygenation on vascular reactivity to angiotensin II and angiotensin-(1-7) in rats",
abstract = "Objective: To assess and elucidate the mechanisms of hyperbaric oxygenation (HBO2) effects on vascular reactivity to angiotensin-(1-7) [ANG-(1-7)] and angiotensin II (ANG II). Methods: Rat aortic rings (HBO 2 vs. control group) were used to test responses to ANG II, ANG II+ ANG-(1-7) or ANG-(1-7) after noradrenaline precontraction in the presence/absence of MS-PPOH, a specific CYP 450-epoxygenase inhibitor, and glibenclamide, a KAT P channels inhibitor. mRNA expression studies of specific CYP isozymes have been conducted as well. Results: The mean contraction (expressed as percent of maximal contraction) for ANG II was similar between groups. Contraction for ANG II + ANG-(1-7) was 15{\%} ± 10 (HBO2) and 20{\%} ± 9 (control). There was a significant decrease between the contraction response to ANG II (HBO2) and the response to ANG II + ANG-(1-7) in the HBO2 group, without such a difference within the control group. Mean percentage of noradrenaline precontraction decrease after ANG-(1-7) addition was significantly different [10{\%} ± 9 (control) and 19{\%} ± 11 (HBO2)]. The epoxygenase inhibitor MS-PPOH in HBO2 animals reversed these changes. Glibenclamide had no effect on relaxation in response to ANG-(1-7). Expression of CYP4A2, CYP4A3 and CYP2J3 mRNA was not significantly altered with HBO, whereas CYP4A1 was significantly upregulated. Conclusions: Our results suggest a role for epoxyeicosatrienoic acids in modulating relaxation response to ANG-(1-7) with HBO2 that is conducted via potassium channels other than K AT P channels. HBO2 increased the responses to ANG-(1-7) after precontraction with noradrenaline. The difference between the response to ANG II in the HBO2 group and ANG II + ANG-(1-7) in the HBO 2 group (the contraction force of the peptide combination being lower), without such difference in the control group, suggests an influence of HBO2 on vascular reactivity.",
author = "Aleksandar Kibel and Ana Cavka and Anita Cosic and Falck, {J R} and Ines Drenjancevic",
year = "2012",
month = "11",
language = "English (US)",
volume = "39",
pages = "1053--1066",
journal = "Undersea and Hyperbaric Medicine",
issn = "1066-2936",
publisher = "Undersea and Hyperbaric Medical Society",
number = "6",

}

TY - JOUR

T1 - Effects of hyperbaric oxygenation on vascular reactivity to angiotensin II and angiotensin-(1-7) in rats

AU - Kibel, Aleksandar

AU - Cavka, Ana

AU - Cosic, Anita

AU - Falck, J R

AU - Drenjancevic, Ines

PY - 2012/11

Y1 - 2012/11

N2 - Objective: To assess and elucidate the mechanisms of hyperbaric oxygenation (HBO2) effects on vascular reactivity to angiotensin-(1-7) [ANG-(1-7)] and angiotensin II (ANG II). Methods: Rat aortic rings (HBO 2 vs. control group) were used to test responses to ANG II, ANG II+ ANG-(1-7) or ANG-(1-7) after noradrenaline precontraction in the presence/absence of MS-PPOH, a specific CYP 450-epoxygenase inhibitor, and glibenclamide, a KAT P channels inhibitor. mRNA expression studies of specific CYP isozymes have been conducted as well. Results: The mean contraction (expressed as percent of maximal contraction) for ANG II was similar between groups. Contraction for ANG II + ANG-(1-7) was 15% ± 10 (HBO2) and 20% ± 9 (control). There was a significant decrease between the contraction response to ANG II (HBO2) and the response to ANG II + ANG-(1-7) in the HBO2 group, without such a difference within the control group. Mean percentage of noradrenaline precontraction decrease after ANG-(1-7) addition was significantly different [10% ± 9 (control) and 19% ± 11 (HBO2)]. The epoxygenase inhibitor MS-PPOH in HBO2 animals reversed these changes. Glibenclamide had no effect on relaxation in response to ANG-(1-7). Expression of CYP4A2, CYP4A3 and CYP2J3 mRNA was not significantly altered with HBO, whereas CYP4A1 was significantly upregulated. Conclusions: Our results suggest a role for epoxyeicosatrienoic acids in modulating relaxation response to ANG-(1-7) with HBO2 that is conducted via potassium channels other than K AT P channels. HBO2 increased the responses to ANG-(1-7) after precontraction with noradrenaline. The difference between the response to ANG II in the HBO2 group and ANG II + ANG-(1-7) in the HBO 2 group (the contraction force of the peptide combination being lower), without such difference in the control group, suggests an influence of HBO2 on vascular reactivity.

AB - Objective: To assess and elucidate the mechanisms of hyperbaric oxygenation (HBO2) effects on vascular reactivity to angiotensin-(1-7) [ANG-(1-7)] and angiotensin II (ANG II). Methods: Rat aortic rings (HBO 2 vs. control group) were used to test responses to ANG II, ANG II+ ANG-(1-7) or ANG-(1-7) after noradrenaline precontraction in the presence/absence of MS-PPOH, a specific CYP 450-epoxygenase inhibitor, and glibenclamide, a KAT P channels inhibitor. mRNA expression studies of specific CYP isozymes have been conducted as well. Results: The mean contraction (expressed as percent of maximal contraction) for ANG II was similar between groups. Contraction for ANG II + ANG-(1-7) was 15% ± 10 (HBO2) and 20% ± 9 (control). There was a significant decrease between the contraction response to ANG II (HBO2) and the response to ANG II + ANG-(1-7) in the HBO2 group, without such a difference within the control group. Mean percentage of noradrenaline precontraction decrease after ANG-(1-7) addition was significantly different [10% ± 9 (control) and 19% ± 11 (HBO2)]. The epoxygenase inhibitor MS-PPOH in HBO2 animals reversed these changes. Glibenclamide had no effect on relaxation in response to ANG-(1-7). Expression of CYP4A2, CYP4A3 and CYP2J3 mRNA was not significantly altered with HBO, whereas CYP4A1 was significantly upregulated. Conclusions: Our results suggest a role for epoxyeicosatrienoic acids in modulating relaxation response to ANG-(1-7) with HBO2 that is conducted via potassium channels other than K AT P channels. HBO2 increased the responses to ANG-(1-7) after precontraction with noradrenaline. The difference between the response to ANG II in the HBO2 group and ANG II + ANG-(1-7) in the HBO 2 group (the contraction force of the peptide combination being lower), without such difference in the control group, suggests an influence of HBO2 on vascular reactivity.

UR - http://www.scopus.com/inward/record.url?scp=84872937333&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84872937333&partnerID=8YFLogxK

M3 - Article

VL - 39

SP - 1053

EP - 1066

JO - Undersea and Hyperbaric Medicine

JF - Undersea and Hyperbaric Medicine

SN - 1066-2936

IS - 6

ER -