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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+/-1 mmHg p<0.01, in diastolic BP by 2+/-0.6 mmHg 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+/-1.9 mmHg (NS), diastolic BP by 2+/-1 mmHg 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+/-0.6 mmHg 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.

The objective of our study was to compare the cardiovascular effects of moderate exercise training in healthy young (NTS, n=18, 22.9+/-0.44 years) and in hypertensive human subjects (HTS, n=30, 23+/-1.1). The VO(2max) did not significantly differ between groups. HTS of systolic blood pressure (SBP) 148+/-3.6 mmHg and diastolic blood pressure(DBP) 88+/-2.2 mmHg, and NTS of SBP: 128.8 +/- 4 mmHg and DBP: 72 +/- 2.9 mmHg were submitted to moderate dynamic exercise training, at about 50% VO(2max) 3 times per week for one hour, over 3 months. VO(2max) 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 VO(2max) 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 (LF(SPB)) 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 LF(SPB) in trained hypertensive subjects normalized to the resting level of LF(SPB) in NTS. Our findings suggest that antihypertensive hemodynamic effects of moderate dynamic physical training are associated with readjustment of the autonomic cardiovascular control system.

Hemodynamic consequences of the withdrawal of arterial chemoreceptor drive (ACD) by brief systemic hyperoxia were studied in 16 mild hypertensive subjects (HT) and in 16 healthy subjects (NT) in horizontal position at resting metabolic rate. In another 9 mild HT and match NT measurements were made in resting sitting position and during steady-state mild physical exercise on cycloergometer, (30% of VO2 max.) Tidal volume, minute ventilation, end tidal CO2 and O2 concentration, K+, Na+, pO2, pCO2 values in blood were recorded. Impedance reography was used for recording stroke volume (SV) and arm blood flow (ABF). Cardiac output (CO), ABF and arterial blood pressure (ABF) values were used for calculation of the total peripheral resistance (TPR) and vascular resistance in the arm (AVR). To assess the neurogenic circulatory response to withdrawal of ACD in HT attenuated by opposite peripheral effects of high oxygen, the values of AVR, ABP, TPR and AVR changes during brief hyperoxia in NT, assumed to be of peripheral origin, were subtracted from respective values in HT, assumed to be of mixed neurogenic and peripheral origin. In HT hyperoxia applied in sitting position produced a brief decrease in systolic and diastolic ABP by 5.4 +/- 0.8% and 3.4 +/- 1.1% respectively, of TPR by 12.4 +/- 3% and of AVR by 4.7 +/- 4.6%. Decrease in AVR during hyperoxia was significantly greater in sitting than in horizontal position. In NT hyperoxia produced opposite effects in ABP, TPR and AVR, as compared to those in HT. In HT subjects during steady-state exercise the TPR decreased by 21 +/- 3.7% reaching a value no different from that in NT. We suggest, that in primary hypertension neurogenic sympathoexcitatory ACD is augmented and interacts with the peripheral mechanisms related to tissue oxygen supply.

The effects of clonidine (1.5 mcg/kg of body weight), L-DOPA (4 mg/kg) and propranolol (0.1 mg/kg) on the reflex bradycardia caused by stimulation of the arterial baroreceptors were studied in 46 waking cats in encephale isole preparations. The drugs were administered into the vertebral artery. They increased the gain of the cardiovagal reflex from the arterial baroreceptors by 162%, 162.5%, 150% respectively with regard to the control values. A similar effect of clonidine and propranolol was manifested also in cats with spinal cord destroyed between the segments C1 to Th12. The effects of clonidine and L-DOPA on the cardiovagal component of the reflex were abolished by aceperon (4 mg/kg) injected into the vertebral artery.