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Theophylline-induced endothelium-dependent vasodilation is mediated by increased nitric oxide release and phosphodiesterase inhibition in rat aortaopen access

Authors
Park, Kyeong-EonLee, Soo HeeIl Bae, SungHwang, YeranOk, Seong-HoAhn, Seung HyunSim, GyujinChung, SoongheeSohn, Ju-Tae
Issue Date
Oct-2023
Publisher
AEPRESS SRO
Keywords
Theophylline; Nitric oxide; Endothelium; Phosphodiesterase; Vasodilation
Citation
GENERAL PHYSIOLOGY AND BIOPHYSICS, v.42, no.6, pp 469 - 478
Pages
10
Indexed
SCIE
SCOPUS
Journal Title
GENERAL PHYSIOLOGY AND BIOPHYSICS
Volume
42
Number
6
Start Page
469
End Page
478
URI
https://scholarworks.gnu.ac.kr/handle/sw.gnu/68618
DOI
10.4149/gpb_2023023
ISSN
0231-5882
1338-4325
Abstract
This study aimed to examine the endothelial dependence of vasodilation induced by the phosphodiesterase inhibitor theophylline in isolated rat thoracic aortas and elucidate the underlying mechanism, with emphasis on endothelial nitric oxide (NO). The effects of various inhibitors and endothelial denudation on theophylline-induced vasodilation, and the effect of theophylline on vasodilation induced by NO donor sodium nitroprusside, cyclic guanosine monophosphate (cGMP) analog bromo-cGMP, and beta-agonist isoproterenol in endothelium -denuded aorta were examined. The effects of theophylline and sodium nitroprusside on cGMP formation were also examined. We examined the effect of theophylline on endothelial nitric oxide synthase (eNOS) phosphorylation and intracellular calcium levels. Theophylline-induced vasodilation was greater in endothelium-intact aortas than that in endothelium-denuded aortas. The NOS inhibitor, NW-nitro-L-arginine methyl ester; non-specific guanylate cyclase (GC) in-hibitor, methylene blue; and NO-sensitive GC inhibitor, 1H-[1,2,4]oxadiazolo[4,3-a] quinoxalin-1-one inhibited theophylline-induced vasodilation in endothelium-intact aortas. Theophylline increased the vasodilation induced by sodium nitroprusside, bromo-cGMP, and isoproterenol. Theophylline increased cGMP formation in endothelium-intact aortas, and sodium nitroprusside-induced cGMP formation in endothelium-denuded aortas. Moreover, theophylline increased stimulatory eNOS (Ser1177) phosphorylation and endothelial calcium levels, but decreased the phosphorylation of inhibitory eNOS (Thr495). These results suggested that theophylline-induced endothelium-dependent vasodilation was mediated by increased endothelial NO release and phosphodiesterase inhibition.
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