PURPOSE: Vasodilatation is a frequent side effect of radiographic contrast media, partially due to a direct effect on vascular smooth muscles. Our purpose was therefore to examine any possible implication of the cyclic adenosine monophospate (cAMP) and cyclic guanosine monophosphate (cGMP) pathways in contrast media induced vasorelaxation. MATERIAL AND METHODS: Isolated segments of swine renal arteries were precontracted with 10 microM phenylephrine and relaxed with iomeprol before and after blockade of the cAMP and cGMP pathways. RESULTS: 80 mM and 160 mM of iomeprol significantly relaxed about 52% and 68% of the precontracted arterial rings, respectively. 10 microM of IBMX, a phosphodiesterase inhibitor, did not increase the relaxant effect of 80 mM iomeprol but increased the relaxations induced by 400 nM forskolin by about 1.9 times (which stimulates the production of cAMP), and by 1 microM sodium nitroprusside (which stimulates the production of cGMP). 1 microM of H89 (an inhibitor of the cAMP-dependent protein kinase), was able to reduce the relaxation induced by 4 microM forskolin by about 2.5 times but had no significant effect on the relaxation induced by 160 mM iomeprol. 10 microM of ODQ (an inhibitor of the soluble guanylate cyclase), could reduce the relaxation induced by 10 microM of SNP but not the one induced by 160 mM iomeprol. Moreover, the absence of endothelial cells did not alter the relaxation induced by iomeprol. CONCLUSION: The activation of the cAMP and cGMP pathways are not involved in the in vitro relaxation induced by iomeprol in swine renal arteries.
PURPOSE: Vasodilatation is a frequent side effect of radiographic contrast media, partially due to a direct effect on vascular smooth muscles. Our purpose was therefore to examine any possible implication of the cyclic adenosine monophospate (cAMP) and cyclic guanosine monophosphate (cGMP) pathways in contrast media induced vasorelaxation. MATERIAL AND METHODS: Isolated segments of swine renal arteries were precontracted with 10 microM phenylephrine and relaxed with iomeprol before and after blockade of the cAMP and cGMP pathways. RESULTS: 80 mM and 160 mM of iomeprol significantly relaxed about 52% and 68% of the precontracted arterial rings, respectively. 10 microM of IBMX, a phosphodiesterase inhibitor, did not increase the relaxant effect of 80 mM iomeprol but increased the relaxations induced by 400 nM forskolin by about 1.9 times (which stimulates the production of cAMP), and by 1 microM sodium nitroprusside (which stimulates the production of cGMP). 1 microM of H89 (an inhibitor of the cAMP-dependent protein kinase), was able to reduce the relaxation induced by 4 microM forskolin by about 2.5 times but had no significant effect on the relaxation induced by 160 mM iomeprol. 10 microM of ODQ (an inhibitor of the soluble guanylate cyclase), could reduce the relaxation induced by 10 microM of SNP but not the one induced by 160 mM iomeprol. Moreover, the absence of endothelial cells did not alter the relaxation induced by iomeprol. CONCLUSION: The activation of the cAMP and cGMP pathways are not involved in the in vitro relaxation induced by iomeprol in swine renal arteries.