A photosensitive vascular smooth muscle store of nitric oxide in mouse aorta: No dependence on expression of endothelial nitric oxide synthase

Karen L. Andrews, John J. McGuire, Christopher Triggle

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

1. Photorelaxation is the reversible relaxation of vascular smooth muscle (VSM) when irradiated with ultraviolet (UV) light resulting from the release of nitric oxide (NO). In this study we characterize the involvement of endothelial nitric oxide synthase (eNOS) in the photorelaxation response of thoracic aorta from endothelial NOS deficient (-/-) and control (C57BL/6j) mice. 2. Cirazoline contracted aortae were repeatedly exposed to 30 s of UV light every 3-4 min. Equal levels of photorelaxation (45 ± 2%; n = 34) was observed in both strains. 3. 1H-[1,2,4]-oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), K+, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (c-PTIO), 4-aminopyridine (4-AP) and ethacrynic acid significantly reduced the photorelaxation response. In C57BL/6j mice diethyldithiocarbamate (DETCA) also reduced photorelaxation. 4. Control endothelium-intact and -denuded aorta and L-NAME (100 μM) treated and untreated eNOS (-/-) aortae were repeatedly exposed to UV light for 5 min every 10 min until no photorelaxation response was observed. After 1 h of rest in the dark the vessels showed between 30-70% recovery of the photorelaxation response indicating regeneration of the store in the absence of the endothelium and eNOS. 5. The results of this study suggest that photorelaxation in mouse aorta VSM results from the release of NO from a stable store of RSNOs, which activates soluble guanylate cyclase (sGC), leading to cGMP-dependent relaxation that is partially mediated by an increase in Kv channel activation and hyperpolarization. In addition, the eNOS isoform is not essential for the formation of the photorelaxation store and a non-NOS source of NO may be involved in the maintenance of this store.

Original languageEnglish
Pages (from-to)932-940
Number of pages9
JournalBritish Journal of Pharmacology
Volume138
Issue number5
DOIs
Publication statusPublished - 2003
Externally publishedYes

Fingerprint

Nitric Oxide Synthase Type III
Vascular Smooth Muscle
Aorta
Nitric Oxide
Ultraviolet Rays
Inbred C57BL Mouse
Endothelium
Ethacrynic Acid
Ditiocarb
4-Aminopyridine
NG-Nitroarginine Methyl Ester
Thoracic Aorta
Regeneration
Protein Isoforms
Maintenance

Keywords

  • ENOS deficient mice
  • Mouse aorta
  • Photorelaxation
  • S-nitrosothiols
  • UV light

ASJC Scopus subject areas

  • Pharmacology

Cite this

A photosensitive vascular smooth muscle store of nitric oxide in mouse aorta : No dependence on expression of endothelial nitric oxide synthase. / Andrews, Karen L.; McGuire, John J.; Triggle, Christopher.

In: British Journal of Pharmacology, Vol. 138, No. 5, 2003, p. 932-940.

Research output: Contribution to journalArticle

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abstract = "1. Photorelaxation is the reversible relaxation of vascular smooth muscle (VSM) when irradiated with ultraviolet (UV) light resulting from the release of nitric oxide (NO). In this study we characterize the involvement of endothelial nitric oxide synthase (eNOS) in the photorelaxation response of thoracic aorta from endothelial NOS deficient (-/-) and control (C57BL/6j) mice. 2. Cirazoline contracted aortae were repeatedly exposed to 30 s of UV light every 3-4 min. Equal levels of photorelaxation (45 ± 2{\%}; n = 34) was observed in both strains. 3. 1H-[1,2,4]-oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), K+, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (c-PTIO), 4-aminopyridine (4-AP) and ethacrynic acid significantly reduced the photorelaxation response. In C57BL/6j mice diethyldithiocarbamate (DETCA) also reduced photorelaxation. 4. Control endothelium-intact and -denuded aorta and L-NAME (100 μM) treated and untreated eNOS (-/-) aortae were repeatedly exposed to UV light for 5 min every 10 min until no photorelaxation response was observed. After 1 h of rest in the dark the vessels showed between 30-70{\%} recovery of the photorelaxation response indicating regeneration of the store in the absence of the endothelium and eNOS. 5. The results of this study suggest that photorelaxation in mouse aorta VSM results from the release of NO from a stable store of RSNOs, which activates soluble guanylate cyclase (sGC), leading to cGMP-dependent relaxation that is partially mediated by an increase in Kv channel activation and hyperpolarization. In addition, the eNOS isoform is not essential for the formation of the photorelaxation store and a non-NOS source of NO may be involved in the maintenance of this store.",
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N2 - 1. Photorelaxation is the reversible relaxation of vascular smooth muscle (VSM) when irradiated with ultraviolet (UV) light resulting from the release of nitric oxide (NO). In this study we characterize the involvement of endothelial nitric oxide synthase (eNOS) in the photorelaxation response of thoracic aorta from endothelial NOS deficient (-/-) and control (C57BL/6j) mice. 2. Cirazoline contracted aortae were repeatedly exposed to 30 s of UV light every 3-4 min. Equal levels of photorelaxation (45 ± 2%; n = 34) was observed in both strains. 3. 1H-[1,2,4]-oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), K+, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (c-PTIO), 4-aminopyridine (4-AP) and ethacrynic acid significantly reduced the photorelaxation response. In C57BL/6j mice diethyldithiocarbamate (DETCA) also reduced photorelaxation. 4. Control endothelium-intact and -denuded aorta and L-NAME (100 μM) treated and untreated eNOS (-/-) aortae were repeatedly exposed to UV light for 5 min every 10 min until no photorelaxation response was observed. After 1 h of rest in the dark the vessels showed between 30-70% recovery of the photorelaxation response indicating regeneration of the store in the absence of the endothelium and eNOS. 5. The results of this study suggest that photorelaxation in mouse aorta VSM results from the release of NO from a stable store of RSNOs, which activates soluble guanylate cyclase (sGC), leading to cGMP-dependent relaxation that is partially mediated by an increase in Kv channel activation and hyperpolarization. In addition, the eNOS isoform is not essential for the formation of the photorelaxation store and a non-NOS source of NO may be involved in the maintenance of this store.

AB - 1. Photorelaxation is the reversible relaxation of vascular smooth muscle (VSM) when irradiated with ultraviolet (UV) light resulting from the release of nitric oxide (NO). In this study we characterize the involvement of endothelial nitric oxide synthase (eNOS) in the photorelaxation response of thoracic aorta from endothelial NOS deficient (-/-) and control (C57BL/6j) mice. 2. Cirazoline contracted aortae were repeatedly exposed to 30 s of UV light every 3-4 min. Equal levels of photorelaxation (45 ± 2%; n = 34) was observed in both strains. 3. 1H-[1,2,4]-oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), K+, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (c-PTIO), 4-aminopyridine (4-AP) and ethacrynic acid significantly reduced the photorelaxation response. In C57BL/6j mice diethyldithiocarbamate (DETCA) also reduced photorelaxation. 4. Control endothelium-intact and -denuded aorta and L-NAME (100 μM) treated and untreated eNOS (-/-) aortae were repeatedly exposed to UV light for 5 min every 10 min until no photorelaxation response was observed. After 1 h of rest in the dark the vessels showed between 30-70% recovery of the photorelaxation response indicating regeneration of the store in the absence of the endothelium and eNOS. 5. The results of this study suggest that photorelaxation in mouse aorta VSM results from the release of NO from a stable store of RSNOs, which activates soluble guanylate cyclase (sGC), leading to cGMP-dependent relaxation that is partially mediated by an increase in Kv channel activation and hyperpolarization. In addition, the eNOS isoform is not essential for the formation of the photorelaxation store and a non-NOS source of NO may be involved in the maintenance of this store.

KW - ENOS deficient mice

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KW - S-nitrosothiols

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