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Long‐lasting cyclic guanosine‐3‘,5’ ‐monophosphate accumulation in the medium of cultured smooth muscle cells from atherosclerotic rabbit aortas in response to exogenous or endogenous nitric oxide
Author(s) -
Rupin Alain,
BehrRoussel Delphine,
Verbeuren Tony J.
Publication year - 2000
Publication title -
fundamental and clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.655
H-Index - 73
eISSN - 1472-8206
pISSN - 0767-3981
DOI - 10.1111/j.1472-8206.2000.tb00427.x
Subject(s) - sodium nitroprusside , soluble guanylyl cyclase , nitric oxide , extracellular , vascular smooth muscle , intracellular , endogeny , nitric oxide synthase , chemistry , guanosine , cyclic guanosine monophosphate , medicine , endocrinology , snap , biology , biochemistry , smooth muscle , cyclic gmp , computer graphics (images) , computer science
— Although atherosclerosis causes a marked inhibition of the endothelium‐dependent vasorelaxation it also leads to expression of inducible nitric oxide synthase (iNOS), accompanied by an increase in cyclic GMP content, in the arterial wall. The aim of our present study was to evaluate the influence of atherosclerosis on the soluble guanylyl cyclase pathway in viable cultured smooth muscle cells (SMC) from rabbit atherosclerotic rabbit aortas (atherosclerotic SMC) and from control rabbit aortas (control SMC). In response to 100 μM sodium nitroprusside (SNP), the intracellular production of cyclic GMP was similar in both types of cells, reaching a maximum after 5 min of incubation. In the culture medium, SNP evokes an increased cyclic GMP concentration lasting 6 h in control SMC and 24 h in atherosclerotic SMC. Interleukin‐1 β (100 IU/mL), which induces iNOS in SMC from both control and atherosclerotic aortas causes accumulation of cyclic GMP in the extracellular medium between 3 and 6 h for control SMC and between 3 and 24 h with atherosclerotic SMC. These results demonstrate a long‐lasting egression of cyclic GMP in the extracellular medium of cultured SMC from rabbit aortas in response to endogenous or exogenous NO. Since this egression of cyclic GMP lasts longer in atherosclerotic than in control SMC. we suggest that atherosclerosis dysregulates the long‐term soluble guanylyl cyclase response to NO in SMC.