Serum nitric oxide synthase activity is a novel predictor of impaired vasorelaxation in rats

Summary It is well documented that both acetylcholine (ACh)‐evoked arterial relaxation and brachial artery flow‐mediated vasodilatation are blunted in hypercholesterolaemic patients. However, there are no simple diagnostic methods to detect the pathology of blood vessels of patients. To establish th...

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Veröffentlicht in:Clinical and experimental pharmacology & physiology 2012-10, Vol.39 (10), p.894-896
Hauptverfasser: Chan, Enoch, Chan, Janet Yuen-Yan, Wu, Jian-Hong, Wan, Chun-Wai, Leung, George Pak-Heng, Lee, Simon Ming-Yuen, Kwan, Yiu-Wa, Chan, Shun-Wan
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Sprache:eng
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Zusammenfassung:Summary It is well documented that both acetylcholine (ACh)‐evoked arterial relaxation and brachial artery flow‐mediated vasodilatation are blunted in hypercholesterolaemic patients. However, there are no simple diagnostic methods to detect the pathology of blood vessels of patients. To establish the use of serum nitric oxide synthase (NOS) activity as a diagnostic parameter for impaired vasorelaxation, animals with different levels of vascular healthiness were made by feeding Sprague–Dawley rats a normal diet, a high‐cholesterol diet (HCD) or an HCD supplemented with 10 mg/kg per day, p.o., simvastatin, a cholesterol‐lowering drug, for 30 days. Serum total cholesterol levels, serum NOS activity and ACh‐induced vasorelaxation of the isolated aorta were determined at the end of the experiment. Consumption of HCD for 30 days resulted in an increase in serum total cholesterol, attenuated ACh‐induced nitric oxide/endothelium‐dependent aortic relaxation and decreased NOS activity. Concomitant administration of simvastatin lowered the elevated blood cholesterol levels with complete reversal of the attenuated ACh‐induced aortic relaxation and serum NOS activity. An attempt was made to correlate serum NOS activity and the magnitude of ACh‐elicited vascular relaxation among the different groups. A positive correlation (r = 0.8329; P 
ISSN:0305-1870
1440-1681
DOI:10.1111/j.1440-1681.2012.05748.x