AI Article Synopsis
- Chronic treatment with DPSPX in rats leads to hypertension and cardiovascular changes, potentially due to accelerated nitric oxide (NO) degradation.
- DPSPX was found to scavenge NO in a concentration-dependent manner, which was assessed using specific assays, while caffeine and DPCPX did not exhibit this effect.
- The reduced urinary excretion of nitrites in DPSPX-treated rats indicates decreased NO availability, suggesting DPSPX's unique role in endothelial dysfunction related to hypertension.
Article Abstract
Chronic treatment of rats with 1,3-dipropyl-8-sulfophenylxanthine (DPSPX), an antagonist of adenosine receptors, causes hypertension, cardiovascular hypertrophy and hyperplasia and impaired endothelium-dependent vasodilatation. An accelerated degradation of nitric oxide (NO) by scavenging molecules could account for endothelial dysfunction and trophic changes in this hypertension. Our aim was to determine whether DPSPX is a scavenger of NO and if this putative effect is shared by caffeine (1,3,7-trimethylxanthine) and DPCPX (1,3-dipropyl-8-ciclopentylxanthine), which are also adenosine receptor antagonists but do not induce hypertension in rats. This effect was evaluated by electrochemical and spectrofluorometric assays. Urinary NOx (nitrate + nitrite) excretion was also evaluated in controls and DPSPX-treated rats as a marker for NO bioavailability. DPSPX behaved as a scavenger of NO in a concentration-dependent manner in the electrochemical and spectrofluorometric assays. Caffeine and DPCPX had no scavenging effect. DPSPX-treated rats had decreased excretion of urinary nitrites. We can conclude that: DPSPX has NO scavenging properties that may be involved in the alterations described for DPSPX-hypertensive rats; this NO-scavenging effect is not shared by caffeine and DPCPX, which are also xanthine derivatives and adenosine antagonists.
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| http://dx.doi.org/10.1211/0022357055614 | DOI Listing |
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