This study examined nitric oxide (NO) production, oxidative load and endothelium-dependent rela xation (NO-depe ndent and NO-independent) in adult male borderline hypertensive (BHR) and spontaneously hypertensive (S HR) rats as compared to normotensive Wistar-Kyoto (WKY) rats. Systolic blood pressure (BP) was determined by tail-cuff. NO production was determined by conversion of [3 H]-L-arginine. Conjugated dienes (CD) and concentrations of thiobarbituric acid-reactive substances (TBARS) were measured for assessment of oxidative load. Vascular function was investigated in ri ngs of the femoral artery (FA) using a wire myograph. BP of WKY, BHR and SHR was 106 ± 2, 143 ± 3 and 191 ± 3 mm Hg, respectively (p<0.01 for each). Significant left ventricle (LV) hy pertrophy and elevated levels of CD and TBARS in the LV were present in BHR and SHR as compared to WKY. NO production was elevated significantly in the aorta of BHR and SHR vs. WKY as well as in the LV of SHR vs. WKY. Acetylcholine (ACh)-induced relaxation of the FA was reduced significantly in both BHR and SHR vs. WKY. The NO-dependent component of ACh-induced relaxation had increasing tendency in hypertensive groups and it correlated positively with BP. The NO-independent component of vasorelaxation was reduced significantly in BHR and SHR vs. WKY and it correlated negatively with BP. In conclusion, the results showed that endothelial dysfunction in the experimental model of borderline hypertensive and hypertensive rats is NO-independent. The results suggest that borderline hypertension represents a risk of other cardiovascular disorders wh ich is qualitatively similar to that of fully developed hypertension., A. Púzserová ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
This study investigated the contribution of reactive oxygen species (ROS) to blood pressure regulation in conscious adult male Wistar rats exposed to acute stress. Role of ROS was investigated in rats with temporally impaired principal blood pressure regulation systems using ganglionic blocker pentolinium (P, 5 mg/kg), angiotensin converting enzyme inhibitor captopril (C, 10 mg/kg), nitric oxide synthase inhibitor L-NAME (L, 30 mg/kg) and superoxide dismutase mimeticum tempol (T,25 mg/kg). Mean arterial pressure (MAP) was measured by
the carotid artery catheter and inhibitors were administered intravenously. MAP was disturbed by a 3-s air jet, which increased MAP by 35.2±3.0 % vs. basal MAP after the first exposure. Air jet increased MAP in captopril-
and tempol-treated rats similarly as observed in saline-treated rats. In pentolinium-treated rats stress significantly decreased MAP vs. pre
-stressvalue. In L-NAME-treated rats stress failed to affect MAP
significantly. Treatment of rats with P+L+C resulted in stress-induced MAP decrease by 17.3±1.3 % vs. pre-stress value and settling time (20.1±4.2 s). In P+L+C+T-treated rats stress led to maximal MAP decrease by 26.4±2.2 % (p<0.005 vs. P+L+C) and prolongation of settling time to 32.6±3.3 s (p<0.05 vs. P+L+C). Area under the MAP curve was significantly smaller in P+L+C-treated rats compared to P+L+C+T-treated ones (167±43 vs. 433±69 a.u., p<0.008). In conclusion, in rats with temporally impaired blood pressure regulation, the lack of ROS resulted in greater stress-induced MAP alterations and prolongation of time required to reach new post-stress steady state.
As wine polyphenols were show n to possess many positive effects in mammals, including improvement of vascular function, this study investigated the effect of the Slovak Alibernet red wine extract (AWE) on blood pressure and vascular function in young normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats. Six weeks old, male, WKY and SHR were treated with AWE for three weeks at the dose of 24.2 mg/kg/day. Blood pressure (BP), determined by tail-cuff plethysmography, was significantly elevated in SHR vs. WKY and AWE failed to affect it. Lipid peroxidation was evaluated by determination of thiobarbituric acid-reactive substances. Vascular function was assessed in rings of the femoral artery using Mulvany-Halpern’s myograph. Maximal endothelium-dependent acetylcholine (ACh)-induced rela xation was reduced in control SHR vs. WKY rats by approximatel y 9.3 %, which was associated with a significant decrease of its NO-independent component. AWE failed to affect maximal AC h-induced relaxation, both its NO-dependent and independen t components, compared to controls of the same genotype. AWE however reduced lipid peroxidation in the left ventricle of both WKY and SHR and in the liver of SHR. In conclusion, three-week administration of AWE failed to reduce BP and to improve endothelial function in the femoral arteries of both genotypes investigated., P. Bališ ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy