We investigated the effect of pertussis toxin (PTX) on hypotensive response induced by acetylcholine (ACh) and bradykinin (BK) and on noradrenaline (NA)-induced pressor response in spontaneously hypertensive rats (SHR). Fifteen-week-old Wistar rats and age-matched SHR were used. Half of SHR received PTX (10 μg/kg/i.v.) and the experiments were performed 48 h later. After the anesthesia the right carotid artery was cannulated in order to record blood pressure (BP). The hypotensive response to ACh was enhanced in SHR compared to Wistar rats. After pretreatment of SHR with PTX the hypotensive response to ACh was reduced compared to untreated SHR and it was also diminished in comparison to Wistar rats. Similarly, the hypotensive response to BK was also decreased after PTX pretreatment. The pressor response to NA was increased in SHR compared to Wistar rats. NA-induced pressor response was considerably decreased after PTX pretreatment compared to untreated SHR. In conclusion, the enhancement of hypotensive and pressor responses in SHR was abolished after PTX pretreatment. Our results suggested that the activation of PTX-sensitive inhibitory Gi proteins is involved in the regulation of integrated vasoactive responses in SHR and PTX pretreatment could be effectively used for modification of BP regulation in this type of experimental hypertension., S. Čačányiová, F. Kristek, J. Kuneš, J. Zicha., and Obsahuje bibliografii a bibliografické odkazy
ncreased systemic vascular resistance is responsible for blood pressure (BP) elevation in most forms of human or experimental hypertension. The enhanced contractility of structurally remodeled resistance arterioles is mediated by enhanced calcium entry (through L type voltagedependent calcium channels - L-VDCC) and/or augmented calcium sensitization (mediated by RhoA/Rho kinase pathway). It is rather difficult to evaluate separately the role of these two pathways in BP control because BP response to the blockade of either pathway is always dependent on the concomitant activity of the complementary pathway. Moreover, vasoconstrictor systems enhance the activity of both pathways, while vasodilators attenuate them. The basal fasudil-sensitive calcium sensitization determined in rats deprived of endogenous renin-angiotensi n system (RAS) and sympathetic nervous system (SNS) in wh ich calcium entry was dose- dependently increased by L-VDCC opener BAY K8644, is smaller in spontaneously hypertensive rats (SHR) than in normotensive Wistar-Kyoto (WKY) rats. In co ntrast, if endogenous RAS and SNS were present in intact rats, fasudil caused a greater BP fall in SHR than WKY rats. Our in vivo experiments indicated that the endogenous pressor systems (RAS and SNS) augment calcium sensitization mediated by RhoA/Rho kinase pathway, whereas the endogenous vasodilator systems (such as nitric oxide) attenuate this pathway. However, the modulation of calcium entry and calcium sensitization by nitric oxide is strain-dependent because NO deficiency significan tly augments low calcium entry in WKY and low calcium sensitization in SHR. Further in vivo and in vitro experiments should clarify the interrelationships between endogenous vasoactive systems an d the contribution of calcium entry and/or calcium sensitization to BP maintenance in various forms of experimental hypertension., J. Zicha ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
The aim of this study was to obtain a detailed analysis of the relationship between the finger arterial compliance C [ml/mm Hg] and the arterial transmural pressure Pt [mm Hg]. We constructed a dynamic plethysmograph enabling us to set up a constant pressure Pcss [mm Hg] and a superimposed fast pressure vibration in the finger cuff (equipped with a source of infra-red light and a photoelectric sensor for the measurement of arterial volume). Pcss could be set on the required time interval in steps ranging between 30 and 170 mm Hg, and on sinusoidal pressure oscillation with an amplitude Pca (2 mm Hg) and a frequency f (20, 25, 30, 35, 40 Hz). At the same time continuous blood pressure BP was measured on the adjacent finger (Portapres). We described the volume dependence of a unitary arterial length on the time-varying transmural pressure acting on the arterial wall (externally Pcss+Pca.sin(2πf), internally BP) by a second-order differential equation for volume. This equation was linearized within a small range of selected BP. In the next step, a Fourier transform was applied to obtain the frequency characteristic in analytic form of a complex linear combination of frequency functions. While series of oscillations [Pca, f] were applied for each Pcss, the corresponding response of the plethysmogram was measured. Amplitude spectra were obtained to estimate coefficients of the frequency characteristic by regression analysis. We determined the absolute value: elastance E, and its inverse value: compliance (C=1/E). Then, C=C(Pt) was acquired by applying sequences of oscillations for different Pcss (and thus Pt) by the above-described procedure. This methodology will be used for the study of finger arterial compliance in different physiological and pathological conditions., J. Moudr, J. Svačinová, E. Závodná, N. Honzíková., and Obsahuje bibliografii
Spontaneously hypertensive rats (SHR/NIH strain) harbor a deletion variant in the Cd36 fatty acid transporter and display defective fatty acid metabolism, insulin resistance and hypertension. Transgenic rescue of Cd36 in SHR ameliorates insulin resistance and improves dyslipidemia. However, the role of Cd36 in blood pressure regulation remains controversial due to inconsistent blood pressure effects that were observed with transgenic expression of Cd36 on the SHR background. In the current studies, we developed two new SHR transgenic lines, which express wild type Cd36 under the control of the universal Ef-1 promoter, and examined the effects of transgenic expression of wild type Cd36 on selected metabolic and cardiovascular phenotypes. Transgenic expression of Cd36 in the new lines was associated with significantly decreased serum fatty acids, amelioration of insulin resistance and glucose intolerance but failed to induce any consistent changes in blood pressure as measured by radiotelemetry. The current findings confirm the genetic association of defective Cd36 with disordered insulin action and fatty acid metabolism in the SHR/NIH strain and suggest that Cd36 is linked to other gene(s) on rat chromosome 4 that regulate blood pressure., M. Pravenec, V. Landa, V. Zídek, A. Musilová, L. Kazdová, N. Qi, J. Wang, E. St.Lezin, T. W. Kurtz., and Obsahuje bibliografii
The aim of our study was to evaluate the potential differences in blood pressure (BP) profile in subjects with different forms of primary aldosteronism (PA). Simultaneously, we studied the effects of PA treatment on BP curve. We therefore monitored 24-hour ambulatory blood pressure values in 22 subjects with aldosterone-producing adenoma (APA), 22 subjects with idiopathic hyperaldosteronism (IHA) and 33 subjects with essential hypertension (EH) as controls. We found a significantly attenuated nighttime systolic BP decline in the APA group (P=0.02). Patients with IHA had lower nighttime systolic BP values (P=0.01) and also a diastolic BP decline (P=0.02) during the night in comparison with EH. We did not detect any significant differences in BP profile characteristics between APA and IHA. Specific treatment of primary aldosteronism (adrenalectomy, treatment with spironolactone) led to the normalization of the BP curve with a marked BP decline. Our study thus demonstrates a blunted diurnal BP variability in patients with primary aldosteronism the specific treatment of which normalized previously attenuated nocturnal BP fall., T. Zelinka, J. Widimský., and Obsahuje bibliografii
Studies have shown that uridine concentration in plasma may be an indicator of uric acid production in patients with gout. It has been also postulated that uridine takes part in blood pressure regulation. Since physical exercise is an effective tool in treatment and prevention of cardio-vascular diseases that are often accompanied by hyperuricemia and hypertension, it seemed advisable to attempt to evaluate the relationship between oxypurine concentrations (Hyp, Xan and UA) and that of Urd and BP after physical exercise in healthy subjects. Sixty healthy men (17.2±1.71 years, BMI 23.2±2.31 kg m-2, VO2max 54.7±6.48 ml kg-1 min-1) took part in the study. The subjects performed a single maximal physical exercise on a bicycle ergometer. Blood for analyses was sampled three times: immediately before exercise, immediately after exercise, and in the 30th min of rest. Concentrations of uridine and hypoxanthine, xanthine and uric acid were determined in whole blood using high-performance liquid chromatography. We have shown in this study that the maximal exercise-induced increase of uridine concentration correlates with the post-exercise increase of uric acid concentration and systolic blood pressure. The results of our study show a relationship between uridine concentration in blood and uric acid concentration and blood pressure. We have been the first to demonstrate that a maximal exercise-induced increase in uridine concentration is correlated with the post-exercise and recovery-continued increase of uric acid concentration in healthy subjects. Thus, it appears that uridine may be an indicator of post-exercise hyperuricemia and blood pressure., W. Dudzinska, A. Lubkowska, B. Dolegowska, M. Suska, M. Janiak., and Obsahuje bibliografii
Cieľom predloženej práce je zhodnotiť vplyv dosiahnutého vzdelania na výskyt metabolického syndrómu a jeho rizikových determinantov u súboru 65 920 klientov poradní zdravia pri 36 regionálnych úradoch verejného zdravotníctva v Slovenskej republike vo veku od 25 rokov. Prítomnosť metabolického syndrómu a jeho rizikových determinantov sme hodnotili podľa kritérií International Diabetes Federation z roku 2005. Celková prevalencia metabolického syndrómu v súbore bola 31,2 %, u mužov 34,9 % a u žien 29,5 %. Úroveň dosiahnutého vzdelania mala menší vplyv na výskyt metabolického syndrómu a jeho rizikových faktorov u mužov ako u žien. Najvýraznejší vplyv vzdelania sme sledovali pri výskyte abdominálnej obezity a metabolického syndrómu u žien, kde ženy so základoškolským vzdelaním mali v priemere 3,14 krát vyššiu šancu mať abdominálnu obezitu (vo vekovej skupine 55–64 ročných žien až 4,17 krát) a v priemere 2,55 krát vyššiu šancu mať metabolický syndróm (vo vekovej skupine 25–34 ročných žien až 3,50 krát) v porovnaní so ženami s vysokoškolským vzdelaním. Výsledky našej štúdie podčiarkujú význam edukácie obyvateľstva s dôrazom na ženy a dôležitosť dosiahnuť aspoň stredoškolské vzdelanie s maturitou, okrem iného aj za účelom zníženia morbidity a mortality na kardiovaskulárne ochorenia na Slovensku., The objective of this work is to evaluate the impact of education level on the incidence of metabolic syndrome and its risk determinants among 65,920 clients of the Health Advice Centres of 36 Regional Public Health Authorities in the Slovak Republic, from the age of 25 years. The presence of metabolic syndrome and its risk determinants were evaluated according to criteria of the International Diabetes Federation from 2005. The overall prevalence of metabolic syndrome in the group was 31.2%, men 34.9% and women 29.5%. Education level has a lower impact on the incidence of metabolic syndrome and its risk factors among men than in women. The most significant effect of the level of education on the occurrence of abdominal obesity and metabolic syndrome we monitored in women. Women with basic level education have on average a 3.14 times higher chance of having abdominal obesity (55–64 years old women up to 4.17 times), and on average a 2.55 times higher chance of having the metabolic syndrome (25–34 years old women up to 3.50 times) compared with women with university education. The results of our study underscore the importance of education of the population with an emphasis on women and the importance of achieving at least secondary education with a "leaving" exam, inter alia, to reduce morbidity and mortality from cardiovascular disease in Slovakia., Tímea Ostrihoňová, Kvetoslava Rimárová, Janka Bérešová, Sylvia Kontrošová, and Literatura