INCREASED NITRIC OXIDE-DEPENDENT COMPONENT OF VASORELAXATION IN NORMOTENSIVE RATS AFTER CHRONIC STRESS: PP.6.233

Abstract

Objective: Previously we showed increased endothelium-dependent vasorelaxation in stressed Wistar-Kyoto (WKY) rats (1) when ascorbic acid (AsA) was present in working physiological salt solution (PSS). The aim of study was to examine endothelium-dependent vasodilatation in the femoral artery (FA) of WKY rats exposed to chronic social stress produced by crowding in absence of AsA in PSS. Design and Method: Adult, male rats were divided into control (480 cm2/rat) or stressed (200 cm2/rat) group for 8 weeks. Blood pressure (BP) and heart rate (HR) were determined using tail-cuff plethysmography. Nitric oxide synthase (NOS) activity was determined by conversion of [3H]-L-arginine. Conjugated dienes (CD) and thiobarbituric acid-reactive substances (TBARS) concentrations were measured in the left ventricle and liver. NO-dependent component of acetylcholine (ACh)-induced, endothelium-dependent relaxation was investigated in the FA pre-constricted with serotonin using the wire myograph as a difference between ACh-induced relaxation before and after acute NOS inhibitor NG-Nitro-L-arginine methyl ester (300 umol/l) pre-treatment. Results: BP and HR were not influenced by chronic stress. NOS activity in the aorta was significantly increased in stressed rats by 80% (p < 0.01) vs. control. ACh-induced relaxation of the FA of stressed rats exceeded that of the controls, which was associated with significant increase of NO-dependent component of relaxation. Similar extent of vasorelaxation was observed when expressed as absolute tension, which indicates an enhancement of NO release after chronic stress. Stress failed to alter sodium nitroprusside-induced relaxation. Additionally, CD and TBARS concentrations were similar in stressed and control rats in both tissues investigated. Conclusions: Data showed better NO bioavailability in the FA of stressed rats resulting in improved vasorelaxation in spite of the absence of AsA in PS S. Thus, the results proved that elevation of NO production during stress exposure is an important way of adaptation preventing normotensive rats from the development of the stress-induced hypertension.