Abstract
Nitric oxide (NO) is a biological messenger that is known to exert a wide range of patho/physiological functions. In particular it is responsible for vasodilation and is well established that the inhibitors of NO synthases (such as L-NAME) induce vascular contraction and hypertension. Vasoconstriction of compliance arteries leads to a potentially harmful increase in heart load. Recently, a new cardiovascular parameter, augmentation index (AIx), has been described to be a biological marker of vascular tree efficiency. The aim of this study was to demonstrate a possible beneficial role of NO in large artery district. To this purpose, we measured AIx in the rat, using a recently developed technical tool enabling arterial pulse wave recording in small rodents (Samba Preclin, Samba Sensors AB, Goteborg, Sweden). To make analysis possible, we used the model of L-NAME-induced hypertension. Pulse wave was recorded in the carotid artery of anesthetized SD rats and drugs were given intravenously by jugular vein cannulation, except for L-NAME that was administered intraperitoneally. L-NAME (50 mg/kg) induced an increase in AIx of 33.9 ± 1.8%, compared to basal value. The NO donor, diethylenetriamine/NO (DETA-NO), 3-morpholinosydnonimine (SIN-1) and isoidide mononitrate (IIMN) (10 mg/kg), significantly decreased AIx (-15.5 ± 4.5%, -40.0 ± 4.93%, -22.7 ± 8.2%, respectively). Also the anti-hypertensive drugs, candesartan (3 mg/kg) and carvedilol (5 mg/kg), counteracted the L-NAME-induced increase in AIx (-16 ± 11% and 4 ± 2%, respectively), while atenolol (30 mg/kg) did not affect the L-NAME effect (data are expressed as delta from basal values). These findings show that NO plays beneficial role in large arteries, suggesting a contribution to heart load reduction. Both NO donors and drugs inducing vasodilation by NO independent pathways (such as candesartan and carvedilol) are able to counteract the increase in large artery vasoconstriction, induced by NO depletion.
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