We aimed to compare the effects of chronic and acute administration of structurally different antihypertensives, diuretics - indapamide and hydrochlorothiazide, ACE inhibitor - captopril and indapamide+captopril combination on endothelium-dependent relaxation of femoral artery isolated from nitric oxide (NO)-deficient rats. In the chronic experiment, femoral artery was isolated from Wistar rats receiving L-NAME (40 mg/kg/day) solely or with indapamide (1 mg/kg/day), hydrochlorothiazide (10 mg/kg/day), captopril (10 mg/kg/day), and indapamide+captopril combination for seven weeks. In the acute in vitro experiment, the incubation medium with femoral artery isolated from L-NAMEhypertensive rats was supplemented with investigated antihypertensives in the same concentration 10-4 mol/l. Interestingly, chronic L-NAME treatment did not cause a reduction of vasorelaxation. Indapamide+captopril elevated relaxation above the control level and completely prevented blood pressure increase induced by L-NAME. Acute incubation with captopril only or indapamide+captopril improved relaxation of femoral artery isolated from L-NAMEhypertensive rats, while the incubation with all antihypertensives increased vasorelaxation of femoral artery isolated from control Wistar rats. In conclusion, NO might be involved in the indapamide- and hydrochlorothiazide-induced improvement of vasorelaxation, while different vasorelaxing factors (prostacyclin, EDHF) contribute to the captoprilinduced improvement of vasorelaxation. During the chronic treatment additive and synergic effects of indapamide and captopril may contribute to the prevention of hypertension and increase of vasorelaxation., M. Sládková, S. Kojšová, L. Jendeková, O. Pecháňová., and Obsahuje bibliografii
The aim of this study was to determine the effect of chronic crowding on the cardiovascular system of Wistar-Kyoto (WKY) rats. Rats were randomly divided into the control (480 cm2 per rat) or crowded (200 cm2 per rat) group for eight weeks. Body weight, blood pressure (BP), heart rate and plasma nitrate/nitrite levels of the crowded rats were not different from controls at the end of the experiment. Plasma corticosterone exhibited an increasing trend (5.7±1.8 vs. 12.6±3.7 ng/ml, p=0.08) while blood glucose was significantly reduced in the crowded rats in comparison with the controls. Nitric oxide (NO) synthase activity and nitrate/nitrite levels of the crowded rats were significantly elevated in the aorta by ∼80 % and ∼20 %, respectively, but unchanged in the left ventricle. Moreover, acetylcholine-induced relaxation was significantly increased in the crowded rats in both the femoral artery (61±5 % vs. 76±5 %, p<0.001) and mesenteric artery (51±6 % vs. 72±7 %, p<0.001). In conclusion, results suggest that chronic crowding may increase vasorelaxation and vascular NO production in normotensive rats. This may be considered as an adapting mechanism preventing the development of the stress-related elevation of BP. Additionally, results also suggest caution in the housing of rats because an inappropriate crowding may affect results of the experiment significantly., I. Bernátová, A. Púzserová, J. Navarová, Z. Csizmadiová, M. Zeman., and Obsahuje bibliografii a bibliografické odkazy
This study aimed to investigate the vasoactivity of sulfur dioxide (SO2), a novel gas identified from vascular tissue, in rat thoracic aorta. The thoracic aorta was isolated, cut into rings, and mounted in organ-bath chambers. After equilibrium, the rings were gradually stretched to a resting tension. Isometric tension was recorded under the treatments with vasoconstrictors, SO2 derivatives, and various drugs as pharmacological interventions. In endothelium-intact aortic rings constricted by 1 μM phenylephrine (PE), SO2 derivatives (0.5 – 8 mM) caused a dose-dependent relaxation. Endothelium removal and a NOS inhibitor L-NAME reduced the relaxation to low doses of SO2 derivatives, but not that to relatively high doses (≥ 2 mM). In endothelium-denuded rings, SO2 derivatives attenuat ed vasoconstriction induced by high K+ (60 mM) or CaCl2 (0.01-10 mM). The relaxation to SO2 derivatives in PE-constricted rings without endothelium was significantly inhibited by blockers of ATP-sensitive K+ (KATP) and Ca2+-activated K+ (KCa) channels, but not by those of voltage-dependent K+ channels, Na+-K+-ATPase or Na+-Ca2+ exchanger. SO2 relaxed vessel tone via endothelium-dependent mechanisms associated with NOS activation, and via endothelium-independent mechanisms dependent on the inhibition of voltage-gated Ca2+ channels, and the opening of KATP and KCa channels., Y.-K- Wang., and Obsahuje seznam literatury