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Study on the involvement of soluble guanylyl cyclase and its different isoforms in carbon monoxide and carbon monoxide releasing molecule-2 induced vasodilatation

Johan Van de Voorde UGent, Kelly Decaluwé UGent, Bart Pauwels UGent, Sara Verpoest UGent and Peter Brouckaert UGent (2011) JOURNAL OF VASCULAR RESEARCH. 48(suppl. 1). p.117-117
abstract
Besides nitric oxide, carbon monoxide (CO) also activates soluble guanylyl cyclase (sGC). CO as well as the CO-donor CORM-2 have been shown to possess vasodilatory properties. Whether these vasodilatory properties by CO can be attributed to sGC activation is still a matter of debate. The aim of this study was to examine the involvement of sGC and its different subunits in CO and CORM-2 induced vasodilatation within different vascular tissues. Isometric tension recordings were performed using mice isolated aortic rings, femoral artery ring segments as well as corpora cavernosa (CC). To be able to distinguish between the different sGC subunits we evaluated responses to saturated CO solutions and CORM-2 in both sGCa1-/- and sGCβ1KI/KI mice and their wild-type controls. Saturated CO solution was unable to relax mice isolated blood vessels, whereas it induced concentration-dependent relaxations in mice CC. In CC of wild-type mice, the response to CO was completely inhibited by the sGC inhibitor ODQ. The involvement of sGC in the CO-induced corporal relaxation was further confirmed by the loss of response to CO in CC isolated from sGCβ1KI/KI mice. Moreover, the vasodilatory responses of CO in the corporal tissue of sGCa1-/- mice were strongly inhibited although not completely abolished. In contrast to CO, CORM-2 was able to relax all vascular tissues examined in the present study, although ODQ only partially blocked the response to CORM-2 in the aorta. Interestingly ODQ did not affect the CORM-2 induced relaxation in the femoral arteries and the CC, indicating that sGC is not involved, which was confirmed using the transgenic mice. This study clearly illustrates that the molecular mechanism of CORM-2 induced vasorelaxation differs from that of CO induced vasorelaxation. While the CO induced vasorelaxation depends on activation of sGC, primarily the sGCa1β1 heterodimer, the vasorelaxing properties of CORM-2 are only partially dependent or even completely independent upon sGC activation. The observation that CO is more effective in relaxing CC tissues than other cardiovascular tissues investigated in the present study suggests that the heme-oxygenase/CO pathway may present a potential new target for therapeutic approaches towards erectile dysfunction.
Please use this url to cite or link to this publication:
author
organization
year
type
conference
publication status
published
subject
in
JOURNAL OF VASCULAR RESEARCH
J. Vasc. Res.
volume
48
issue
suppl. 1
pages
117 - 117
conference name
Joint meeting of the European Society for Microcirculation (ESM) and the Society of Microcirculation and Vascular Biology (GfMVB)
conference location
Munich, Germany
conference start
2011-10-13
conference end
2011-10-16
Web of Science type
Meeting Abstract
Web of Science id
000294760800114
JCR category
PHYSIOLOGY
JCR impact factor
2.651 (2011)
JCR rank
29/78 (2011)
JCR quartile
2 (2011)
ISSN
1018-1172
language
English
UGent publication?
yes
classification
C3
id
1978138
handle
http://hdl.handle.net/1854/LU-1978138
date created
2012-01-04 13:49:49
date last changed
2012-01-09 09:43:03
@inproceedings{1978138,
  abstract     = {Besides nitric oxide, carbon monoxide (CO) also activates soluble guanylyl cyclase (sGC). CO as well as the CO-donor CORM-2 have been shown to possess vasodilatory properties. Whether these vasodilatory properties by CO can be attributed to sGC activation is still a matter of debate. The aim of this study was to examine the involvement of sGC and its different subunits in CO and CORM-2 induced vasodilatation within different vascular tissues. Isometric tension recordings were performed using mice isolated aortic rings, femoral artery ring segments as well as corpora cavernosa (CC). To be able to distinguish between the different sGC subunits we evaluated responses to saturated CO solutions and CORM-2 in both sGCa1-/- and sGC\ensuremath{\beta}1KI/KI mice and their wild-type controls. Saturated CO solution was unable to relax mice isolated blood vessels, whereas it induced concentration-dependent relaxations in mice CC. In CC of wild-type mice, the response to CO was completely inhibited by the sGC inhibitor ODQ. The involvement of sGC in the CO-induced corporal relaxation was further confirmed by the loss of response to CO in CC isolated from sGC\ensuremath{\beta}1KI/KI mice. Moreover, the vasodilatory responses of CO in the corporal tissue of sGCa1-/- mice were strongly inhibited although not completely abolished. In contrast to CO, CORM-2 was able to relax all vascular tissues examined in the present study, although ODQ only partially blocked the response to CORM-2 in the aorta. Interestingly ODQ did not affect the CORM-2 induced relaxation in the femoral arteries and the CC, indicating that sGC is not involved, which was confirmed using the transgenic mice. This study clearly illustrates that the molecular mechanism of CORM-2 induced vasorelaxation differs from that of CO induced vasorelaxation. While the CO induced vasorelaxation depends on activation of sGC, primarily the sGCa1\ensuremath{\beta}1 heterodimer, the vasorelaxing properties of CORM-2 are only partially dependent or even completely independent upon sGC activation. The observation that CO is more effective in relaxing CC tissues than other cardiovascular tissues investigated in the present study suggests that the heme-oxygenase/CO pathway may present a potential new target for therapeutic approaches towards erectile dysfunction.},
  author       = {Van de Voorde, Johan and Decaluw{\'e}, Kelly and Pauwels, Bart and Verpoest, Sara and Brouckaert, Peter},
  booktitle    = {JOURNAL OF VASCULAR RESEARCH},
  issn         = {1018-1172},
  language     = {eng},
  location     = {Munich, Germany},
  number       = {suppl. 1},
  pages        = {117--117},
  title        = {Study on the involvement of soluble guanylyl cyclase and its different isoforms in carbon monoxide and carbon monoxide releasing molecule-2 induced vasodilatation},
  volume       = {48},
  year         = {2011},
}

Chicago
Van de Voorde, Johan, Kelly Decaluwé, Bart Pauwels, Sara Verpoest, and Peter Brouckaert. 2011. “Study on the Involvement of Soluble Guanylyl Cyclase and Its Different Isoforms in Carbon Monoxide and Carbon Monoxide Releasing Molecule-2 Induced Vasodilatation.” In Journal of Vascular Research, 48:117–117.
APA
Van de Voorde, J., Decaluwé, K., Pauwels, B., Verpoest, S., & Brouckaert, P. (2011). Study on the involvement of soluble guanylyl cyclase and its different isoforms in carbon monoxide and carbon monoxide releasing molecule-2 induced vasodilatation. JOURNAL OF VASCULAR RESEARCH (Vol. 48, pp. 117–117). Presented at the Joint meeting of the European Society for Microcirculation (ESM) and the Society of Microcirculation and Vascular Biology (GfMVB).
Vancouver
1.
Van de Voorde J, Decaluwé K, Pauwels B, Verpoest S, Brouckaert P. Study on the involvement of soluble guanylyl cyclase and its different isoforms in carbon monoxide and carbon monoxide releasing molecule-2 induced vasodilatation. JOURNAL OF VASCULAR RESEARCH. 2011. p. 117–117.
MLA
Van de Voorde, Johan, Kelly Decaluwé, Bart Pauwels, et al. “Study on the Involvement of Soluble Guanylyl Cyclase and Its Different Isoforms in Carbon Monoxide and Carbon Monoxide Releasing Molecule-2 Induced Vasodilatation.” Journal of Vascular Research. Vol. 48. 2011. 117–117. Print.