Hyperinsulinaemia may play a causal role in the development of hypertension in obese hypertensives. However, experimental evidence supporting this statement is inappropriate. The main purpose of this study was to evaluate the chronic effects of insulin administration on blood pressure, total-body glucose metabolism and urinary catecholamine excretion. After 10 weeks of insulin injection blood pressure was substantially increased in insulin- treated animals compared to those treated with saline (125±2 vs 108±2 mm Hg, pcO.OOl). There were no differences in glycaemia, plasma triglyceride levels and free fatty acid levels between these two groups. Plasma level of corticosterone was increased in both insulin-treated and saline-treated rats as compared to untreated animals suggesting that the level of stress was similar in both injected groups. The urinary excretion of norepinephrine and dopamine was increased in the insulin-injected group by about 120 % and 310 %, respectively. Our data clearly indicate that long-term insulin administration increased blood pressure but the underlying mechanisms remain to be elucidated.
The relationship between possible alterations in the volume or distribution of extracellular fluid and the development of salt hypertension was studied in inbred salt-sensitive (SS/Jr) and salt-resistant (SR/Jr) Dahl rats. Blood pressure, cardiac and renal hypertrophy as well as body fluid volumes were determined in young and adult SS/Jr and SR/Jr rats of both sexes that were subjected to low, normal or high salt intake for various periods of time. Salt hypertension in young salt-sensitive rats fed a 4 % NaCl diet was not accompanied by any substantial intravascular or interstitial expansion as compared to salt-resistant rats that remained normotensive. There was no sex difference in the response of blood pressure or body fluids to high salt intake. Major expansion of plasma and blood volume, which was elicited by 8 % NaCl diet feeding from prepuberty, was not accompanied by a further blood pressure rise (compared to salt hypertensive SS/Jr rats fed 4 % NaCl diet). In conclusions, salt hypertension can occur in Dahl salt-sensitive rats without major salt and water retention. The degree of intravascular expansion is not directly related to blood pressure levels in salt-loaded Dahl rats. A high salt intake seems to exert its hypertensive effects in Dahl rats preferentially by influencing the balance of vasoconstrictor and vasodilator systems rather than by increasing the haemodynamically active intravascular volume.
We studied the effects of the H2S donor Na2S on the mean arterial blood pressure (MAP) and heart and breathing rates of anesthetized Wistar rats in the presence and absence of captopril. Bolus administration of Na2S (1-4 μmol/kg) into the right jugular vein transiently decreased heart and increased breathing rates; at 8-30 μmol/kg, Na2S had a biphasic effect, transiently decreasing and increasing MAP, while transiently decreasing heart rate and increasing and decreasing breathing rate. These results may indicate independent mechanisms by which H2S influences MAP and heart and breathing rates. The effect of Na2S in decreasing MAP was less pronounced in the presence of captopril (2 μmol/l), which may indicate that the renin-angiotensin system is partially involved in the Na2S effect. Captopril decreased H2S-induced NO release from S-nitrosoglutathione, which may be related to some biological activities of H2S. These results contribute to the understanding of the effects of H2S on the cardiovascular system., M. Drobná, A. Misak, T. Holland, F. Kristek, M. Grman, L. Tomasova, A. Berenyiova, S. Cacanyiova, K. Ondrias., and Obsahuje bibliografii
Our aim was to test the hypothesis that the occurrence of extrasystoles in higher decennia is proportional to the altitude. The occurrence of supraventricular (SVPB) and ventricular (VEB) extrasystoles, values of systolic and diastolic blood pressure and the heart rate were studied in 20 healthy elderly men (50-64 years) during cable cabin transportation to a moderate altitude. These values were measured in stations located at 898 m, 1764 m, and 2632 m above sea level during the transportation in both directions. Our records show that the values of blood pressure and heart rate were within normal limits during the whole period of transportation. Both SVPB and VEB were increasing during the ascent and decreasing to the initial values during the descent compared to the values at altitude of 898 m. The highest values (6 to 7-times exceeding the initial ones) were measured at the summit. The results have demonstrated that the occurrence of SVPB and VEB is proportional to the altitude. The increased incidence in the number of extrasystoles is suggested to be mediated by beta-adrenoceptors., Š. Kujaník, M. Sninčák, K. Galajdová, K. Racková., and Obsahuje bibliografii
Down Syndrome (Ds) is the most common chromosomal cause of intellectual disability that results from triplication of chromosome 21 genes. Individuals with Ds demonstrate cognitive deficits in addition to comorbidities including cardiac defects, pulmonary arterial hypertension (PAH), low blood pressure (BP), and differences in autonomic regulation. Many individuals with Ds are born with heart malformations and some can be surgically corrected. Lower BP at rest and in response to exercise and other stressors are a prevalent feature in Ds. These reduced cardiovascular responses may be due to underlying autonomic dysfunction and have been implicated in lower exercise/work capacity in Ds, which is an important correlate of morbidity, mortality and quality of life. Exercise therapy can be beneficial to normalize autonomic function and may help prevent the development of co-morbidities in Ds. We will review cardiovascular physiology and pathophysiology in individuals with Ds, along with exercise therapy and special considerations for these individuals.
In this study, we investigated the effects of Nw -nitro-L-arginine (L-NNA) on arterial blood pressure (BP), plasma noradrenaline (NA) and adrenaline (A) levels and angiotensin-converting enzyme (ACE) activity. L-NNA was applied with tap water (1 mg/ml) from the 3rd to the 8th week of age (group L-NNA1). In Experiment 1, long-term L-NNA application increased BP compared to the control group (group C1) (L-NNA1 = 131.4 ± 6.3, n=6; C1= 82.7 ± 4.7 mm Hg, n=7) but decreased plasma noradrenaline and adrenaline levels and ACE activity (NA levels: C1 = 15.5 ± 0.8, n=7; L-NNA1= 8,6 ± 0.5 ng/ml, n=7; A levels: C1 = 15.5 ± 0.8, n=7; L-NNA1 = 6.0 ± 0.5 ng/ml, n=7; ACE activities: C1= 87.3 ± 3.1, n=6; L-NNA1 = 46.2 ± 1.9 U/l, n=5). On the other hand, in Experiment 2 (carried out under the same conditions and in age-matched chickens), blood pressure, plasma noradrenaline levels and ACE activity were found to differ in the control group (C2) (BP=141.4 ± 15.5 mm Hg, n=7; NA =1.1 ± 0.4 ng/ml, n=7; ACE = 57.2 ± 5.3 U/l, n=7) as compared to C1, while plasma adrenaline levels were similar. In this series, long-term L-NNA application (group L-NNA2) did not change the BP, but surprisingly increased noradrenaline and ACE values (values of L-NNA2: BP = 165.7 ± 15.6 mm Hg, n=7; NA = 9.3 ± 1.3 ng/ml, n=8; ACE = 149.4 ± 16 U/l, n=8) while decreasing plasma adrenaline levels. L-arginine addition to L-NNA treatment completely reversed plasma noradrenaline and ACE activity values. These results indicate the modulatory activity of an L-arginine-NO pathway on adrenaline release as well as on the renin-angiotensin system in chickens., H. E. Aksulu, I. Bingöl, F. Karatas, H. Sagmanligil, B. Üstündag., and Obsahuje bibliografii
NG-nitro-L-arginine methyl ester (L-NAME) is a non-specific nitric oxide (NO) synthase inhibitor, commonly used for the induction of NO-deficient hypertension. The aim of this study was to investigate the effect of chronic low-dose administration of L-NAME on NO production, vascular function and structure of the heart and selected arteries of rats. Adult male Wistar rats were treated with L-NAME in the dose of approximately 1.5 mg/kg/day in drinking water for 8 weeks. Basal blood pressure (BP) of rats (determined by tail-cuff) was 112±3 mm Hg. The low-dose administration of L-NAME significantly elevated BP measured on the third and sixth week of treatment vs. controls by approximately 9 % and 12 %, respectively. After this period, BP of L-NAME-treated rats returned to the control values. The relative left ventricular mass, heart fibrosis and collagen III/collagen I ratio were not affected by L-NAME. Similarly, there were no alterations in the cross-sectional area and wall thickness/diameter ratio of the aorta and the femoral artery of LNAME- treated rats. NO synthase activity (determined by conversion of [3H]-L-arginine to [3H]-L-citrulline) was not altered in the hypothalamus of L-NAME-treated rats. Interestingly, chronic low-dose L-NAME treatment significantly elevated NO synthase activity in the left ventricle and aorta, increased endothelium-dependent acetylcholine-induced vasorelaxation and reduced serotonin-induced vasoconstriction of the femoral artery. The data suggest that chronic lowdose L-NAME treatment can increase NO production and vasorelaxation in normotensive rats without negative structural changes in the cardiovascular system., I. Bernátová, J. Kopincová, A. Púzserová, P. Janega, P. Babál., and Obsahuje bibliografii
There exists no examination of what is the minimum anti - hypertensive threshold intensity for isometric exercise training. Twenty two normotensive participants were randomly assigned to training intensities at either 5 % or 10 % of their maximal contraction. Twenty participants completed the study. Clinical meaningful, but not statistically significant, reductions in systolic blood pressure were observed in both 5 % and 10 % groups -4.04 mm Hg (95 % CI -8.67 to +0.59, p=0.08) and -5.62 mm Hg (95 % CI -11.5 to +0.29, p=0.06) respectively after 6 weeks training. No diastolic blood pressure reductions were observed in either 5 % -0.97 mm Hg (95 % CI -2.56 to +0.62, p=0.20) or 10 % MVC +1.8 mm Hg (95 % CI -1.29 to +4.89, p=0.22) groups respectively after training. In those unable to complete isometr ic exercise at the traditional 30 % intensity, our results suggest there is no difference between 5 and 10 % groups and based on the principle of regression to the mean, this could mean both interventions induce a similar placebo-effect., N. C. L. Hess, D. J. Carlson, J. D. Inder, E. Jesulola, J. R. McFarlane, N. A. Smart., and Obsahuje bibliografii
Hereditary hypertriglyceridemic (hHTG) rats are characterized by increased blood pressure and impaired endotheliumdependent relaxation of conduit arteries. The aim of this study was to investigate the effect of long-term (4 weeks) treatment of hHTG rats with three drugs which, according to their mechanism of action, may be able to modify the endothelial function: simvastatin (an inhibitor of 3-hydroxy-3-methylglutaryl-CoA reductase), spironolactone (an antagonist of aldosterone receptors) and L-arginine (a precursor of nitric oxide formation). At the end of 4th week the systolic blood pressure in the control hHTG group was 148±2 mm Hg and in control normotensive Wistar group 117±3 mm Hg. L-arginine failed to reduce blood pressure, but simvastatin (118±1 mm Hg) and spironolactone (124±4 mm Hg) treatment significantly decreased the systolic blood pressure. In isolated phenylephrine-precontracted aortic rings from hHTG rats endothelium-dependent relaxation was diminished as compared to control Wistar rats. Of the three drugs used, only simvastatin improved acetylcholine-induced relaxation of the aorta. We conclude that both simvastatin and spironolactone reduced blood pressure but only simvastatin significantly improved endothelial dysfunction of aorta. Prominent increase in the expression of eNOS in large conduit arteries may be the pathophysiological mechanism underlying the protective effect of simvastatin in hHTG rats., J. Török, I. L'upták, J. Matúšková, O. Pecháňová, J. Zicha, J. Kuneš, F. Šimko., and Obsahuje bibliografii
Mitral valve prolapse (MVP) belongs to cardiac disorders characterized by impaired closure of mitral leaflets. We studied adolescent group of patients with MVP suffering from symptomatology that cannot be explained by mitral regurgitation alone. Several studies suggested that symptoms can be explained by autonomic, in particular sympathetic-linked dysfunction. Thus, we assessed non-invasive sympathetic indices of blood pressure and heart rate variability and electrodermal activity (EDA). Fifty-three adolescents with MVP (age: 15.1±0.4 years) and 43 healthy age- and gender-matched adolescents (age: 14.9±0.4 years) were examined. Blood pressure, heart rate and EDA were continuously recorded during 6-min rest. Evaluated parameters were: low frequency band of systolic blood pressure variability, systolic, diastolic and mean blood pressure, mean RR interval, cardiac sympathetic indices: symbolic dynamics (0V%), left ventricular ejection time (LVET), pre-ejection period (PEP), and EDA. Our findings revealed significantly higher systolic, diastolic, and mean blood pressure values, shortened mean RR interval, increased 0V%, and shortened LVET in MVP patients vs. controls (p=0.028, p<0.001, p=0.002, p<0.001, p=0.050, p<0.001; respectively). Our study revealed enhanced cardiovascular sympathetic regulation in adolescent MVP patients. We suggest that evaluation of noninvasive sympathetic parameters could represent potential biomarkers for early diagnosis of cardiovascular complications associated with MVP already at adolescent age.