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We show that force plate measurements provide a noninvasive method to display the motion of the heart muscle and the subsequent propagation of the pulse wave along aorta and its branches. The aim of this paper is to present a new method to handle multivariate time series obtained by force plate measurements. The proposed technique is subsequently used to display marks of cardiac activity.
The objective of our study was to compare the cardiovascular effects of moderate exercise training in heathy young (NTS, n=18, 22.9±0.44 years) and in hypertensive human subjects (HTS, n=30, 23±1.1). The VO2max did not significantly differ between groups. HTS of systolic blood pressure (SBP) 148±3.6 mmHg and diastolic blood pressure(DBP) 88±2.2mmHg, and NTS of SBP: 128.8 ± 4 mmHg and DBP: 72 ± 2.9 mmHg were submitted to moderate dynamic exercise training, at about 50% VO2max 3 times per week for one hour, over 3 months. VO2max was measured by Astrand's test. Arterial blood pressure was measured with Finapres technique, the stroke volume, cardiac output and arm blood flow were assessed by impedance reography. Variability of SBP and pulse interval values (PI) were estimated by computing the variance and power spectra according to FFT algorithm. After training period significant improvements in VO2max were observed in NTS- by 1.92 ±0.76 and in HTS by 3±0.68 ml/kg/min). In HTS significantly decreased: SBP by 19 ±2.9 mmHg, in DBP by 10.7±2 mmHg total peripheral resistance (TPR) by 0.28 ±0.05 TPR units. The pretraining value of low frequency component power spectra SBP (LFSBP) was significantly greater in HTS, compared to NTS. PI variance was lower in HTS, compared to NTS. After physical training, in HTS PI variance increased suggesting a decrease in frequency modulated sympathetic activity and increase in vagal modulation of heart rate in mild hypertension. A major finding of the study is the significant decrease of resting low frequency component SBP power spectrum after training in HTS. The value of LFSBP in trained hypertensive subjects normalized to the resting level of LFSBP in NTS. Our findings suggest that antihypertensive hemodynamic effects of moderate dynamic physical training are associated with readjustment of the autonomic cardiovascular control system.
Both intensive training and bed confinement impair orthostatic tolerance, however, moderate training may exert beneficial effect on cardiovascular adjustment to gravitational stimuli. It was hypothesized that moderate training attenuates effects of bed rest. To test this assumption 24 healthy male volunteers aged 20.8±0.9 yrs were subjected to 6° head down bed rest (HDBR) for 3 days before and after 6 weeks of moderate endurance training. Before and after HDBR graded LBNP tests (-15, -30, -50 mmHg) were performed. During these tests heart rate (HR), stroke volume (SV), blood pressure (BP), plasma catecholamines, ACTH, adrenomedullin, atrial natriuretic peptide, plasma renin activity (PRA) and hematocrit were determined. HDBR did not systematically influence LBNP tolerance up to -50 mmHg, but it enhanced rates of reduction of SV, cardiac output and systolic BP and increased elevations of HR and PRA. Training did not alter significantly effects of HDBR on LBNP-induced changes in HR, SV, CO and TPR but it attenuated decrease in systolic BP and diminished increases in plasma noradrenaline and PRA. In conclusion, training has negligible effect on the HDBR-induced changes in central hemodynamics during LBNP but may increase vascular sensitivity to some vasoconstricting factors.
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The aim of our study was to check the responsiveness the chemoreceptor reflex in 28 young mildly hypertensive men (HTS), aged 18-32 years and 25 normotensive male subjects (NTS) aged 19-32 years, before and after 3-months dynamic exercise training. We tested the hypothesis that dynamic training reduces arterial chemoreceptor drive in mild hypertension. Circulatory response to 3-min hyperoxic inactivation of arterial chemoreceptors induced by 70% oxygen breathing was measured before and after training. Arterial blood pressure (BP) was recorded continuously by Finapres method, stroke volume and arm blood flow were registered by impedance reography, heart rate by ECG. Both groups were submitted to moderate 3-months dynamic exercise training. Before training the hyperoxic breathing caused in HTS a significant decrease in systolic BP by 6±1mmHg p<0.01, in diastolic BP by 2±0.6mmHg p<0.01, and in total peripheral vascular resistance (TPR) by 0.24±0.04 TPRU (p<0.01). After training hyperoxia augmented systolic BP by 2.64±1.9mmHg (NS), diastolic BP by 2±1mmHg p<0.05, and TPR by 0.043±0.05 TPRU (ANOVA). In NTS before training brief hyperoxia produced insignificant change in BP and TPR. In NTS after training hyperoxia increased systolic BP by 4.2 mm Hg±1.23 p<0.01 and diastolic BP by 3.1±0.6mmHg p<0.01 respectively and TPR by 0.053±0.02 TPRU. Our results confirm earlier finding on the enhanced arterial chemoreceptor reflex drive in mild human hypertension. We conclude that normalizing arterial blood pressure in subjects with mild hypertension which occurred after 3-months dynamical exercise training is due to attenuation of the sympathoexcitatory chemoreceptor reflex drive by exercise training. The mechanism of this effect requires further study.
Direct renal nitric oxide (NO) measurements were infrequent and no simultaneous measurements of renal cortical and medullary NO and local perfusion were reported. Large-surface NO electrodes were placed in renal cortex and medulla of anaesthetised rats; simultaneously, renal blood flow (RBF, index of cortical perfusion) and medullary laser-Doppler flux (MBF) were determined. NO synthase inhibitors: nonselective (L-NAME) or selective for neuronal NOS (nNOS) (S-methyl-thiocitrulline, SMTC), and NO donor (SNAP), were used to manipulate tissue NO. Baseline tissue NO was significantly higher in medulla (703±49 nM) than in cortex (231±17 nM). Minimal cortical and medullary NO current measured after maximal L-NAME dose (2.4 mg kg-1 i.v.) was taken as tissue NO zero level. This dose decreased RBF and MBF significantly (-43%). SMTC, 1.2 mg kg-1 h-1 i.v., significantly decreased tissue NO by 105±32 nM in cortex and 546±64 nM in medulla, RBF and MBF decreased 30% and 20%, respectively. Renal artery infusion of SNAP, 0.24 mg kg-1 min-1 significantly increased tissue NO by 139±18 nM in cortex and 948±110 nM in medulla. Since inhibition of nNOS decreased medullary NO by 80% and MBF by 20% only, this isoform has probably minor role in the maintenance of medullary perfusion.
Background: Smooth muscle cells (SMC) constitute the major contractile cell population of blood vessels and inner organs. SMC contraction depends on energy provided by adenosine triphosphate (ATP) catabolism, which can be generated through oxidative phosphorylation in mitochondria or by anaerobic glycolysis. Mitochondrial activity may also modulate smooth muscle tone by biotransformation of vasoactive mediators. Here, we study the role of mitochondrial DNA gene expression for vascular function in vivo. Methods: Since loss of functional mitochondria in SMC may not be compatible with normal development, we generated mice with inducible SMC-specific abrogation of the mitochondrial transcription factor A (Tfam). Deletion of this gene leads to dysfunctional mitochondria and prevents aerobic ATP production in affected cells. Results: Invasive blood pressure monitoring in live animals demonstrated that SMC specific Tfam deletion results in lower blood pressure and a defective blood-pressure response to stress, changes that were not compensated by increased heart rate. The contractility to agonists was reduced in arterial and gastric fundus strips from Tfam-deficient mice. Endothelium-dependent relaxation of arterial strips in response to ACh was also blunted. Conclusion: Our data show that mitochondrial function is needed for normal gastric contraction, vascular tone, and maintenance of normal blood pressure.
Adrenomedullin (ADM) release is enhanced in pheochromocytoma, chronic heart failure (HF), hypertension and renal diseases. This study was designed to test the hypothesis that ADM secretion increases also in response to acute stimuli, such as static effort and to compare plasma ADM response to this stimulus in patients with chronic HF and healthy persons. Eight male HF patients (II/III class NYHA) and eight healthy subjects (C) performed two 3-min bouts of static handgrip at 30% of maximal voluntary contraction, alternately with each hand without any break between the bouts. At the end of both exercise bouts and in 5 min of the recovery period, plasma ADM and catecholamines were determined. In addition, heart rate, blood pressure, and stroke volume (SV) were measured. The baseline plasma ADM and noradrenaline levels were higher, whilst plasma adrenaline and SV were lower in HF patients than in C group. The 1st exercise bout caused an increase in plasma ADM from 3.32 ± 0.57 to 4.98 ± 0.59 pmol l-1 (p<0.01) in C and from 6.88 ± 0.58 to 7.80 ± 0.43 pmol·l-1 (p<0.02) in HF patients. The 2nd exercise bout did not produce further elevation in plasma ADM and during recovery the hormone concentration declined to pre-exercise or lower values. There were no differences between groups in exercise-induced increases in plasma ADM. Plasma ADM correlated with SV (r = -0.419) and with noradrenaline concentrations (r = 0.427). It is concluded that static exercise causes the short-lasting increase in plasma ADM concentration which is similar in healthy subjects and in patients with mild heart failure.
Previous studies from our laboratory have reported a marked reduction in glomerular filtration rate (GFR) and sodium reabsorption in renal proximal tubule during intravenous infusion of P1,P4-diadenosine tetraphosphate (Ap4A) at dose of 1.0 µmol/kg + 10 nmol/kg/min (i.v., injection followed by infusion) in anaesthetized Wistar rats. In the present study, the changes of GFR and urine sodium excretion were investigated in response to systemic infusion of Ap4A at different doses. Ap4A at dose of 0.1 µmol/kg + 1.0 nmol/kg/min did not change GFR and sodium urinary excretion whereas 2-fold higher dose produced significant (3.4-fold) increase in sodium excretion without changes in GFR. Significant but transient reduction in GFR by ~21% was observed during infusion of Ap4A at dose of 0.5 µmol/kg + 5.0 nmol/kg/min. Higher doses of Ap4A (1.0 µmol/kg + 10 nmol/kg/min and 2.0 µmol/kg + 20 nmol/kg/min) produced sustained reduction in GFR and marked natriuresis. Our results suggest that tubular sodium transport systems are more sensitive to Ap4A than systems involved in GFR regulation.
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