High blood pressure (BP) of L-NAME hypertensive rats is maintained not only by the absence of nitric oxide (NO)-dependent vasodilatation but also by the enhancement of both sympathetic and angiotensin II-dependent vasoconstriction. The aim of the present study was to evaluate the role of inhibitory G (Gi) proteins, which are involv ed in tonic sympathetic vasoconstriction, in the pathogenesis of NO-deficient hypertension. We therefore studied BP response to chronic L-NAME administration (60 mg/kg/day for 4 weeks) in rats in which the in vivo inactivation of Gi proteins was induced by injection of pertussis toxin (PTX, 10 μg/kg i.v.). The impairment of sympathetic vasoconstriction due to PTX-induced Gi protein inactivation prevents the full development of NO-deficient hypertension because BP of PTX-treated rats subjected to chronic L-NAME administration did not reach hypertensive values. Nevertheless, chronic NO synthase inhibition per se is capable to increase moderately BP even in PTX-treated rats. Our data suggest that the sympathetic vasoconstriction is essential for the development of established NO-deficient hypertension., J. Zicha ... [et al.]., and Obsahuje seznam literatury
We studied the relationship between blood pressure (BP), body mass index (BMI, kg/m2) and baroreflex sensitivity (BRS, ms/mmHg) in adolescents. We examined 34 subjects aged 16.2±2.4 years who had repeatedly high causal BP (H) and 52 controls (C) aged 16.4±2.2 years. Forty-four C and 22 H were of normal weight (BMI between 19-23.9), and 8 C and 12 H were overweight (BMI between 24-30). Systolic BP was recorded beat-to-beat for 5 min (Finapres, controlled breathing 0.33 Hz). BRS was determined by the cross-spectral method. The predicting power of BMI and BRS for hypertension was evaluated by sensitivity, specificity, and receiver operating curve (ROC - plot of sensitivity versus specificity). H compared with C had lower BRS (p<0.01) and higher BMI (p<0.05). Multiple logistic regression analysis (p<0.001) revealed that a decreased BRS (p<0.05) and an increased BMI (p<0.01) were independently associated with an increased risk of hypertension. No correlation between BMI and BRS was found either in H or in C. Following optimal critical values by ROC, the sensitivity, specificity and area under ROC were determined for: BMI - 22.2 kg/m2, 61.8 %, 69.2 %, 66.0 %; BRS - 7.1 ms/mmHg, 67.7 %, 69.2 %, 70.0 %; BMI and BRS - 0.439 a.u., 73.5 %, 82.7 %, and 77.3 %. Decreased BRS and overweight were found to be independent risk factors for hypertension., K. Krontorádová, N. Honzíková, B. Fišer, Z. Nováková, E. Závodná, H. Hrstková, P. Honzík., and Obsahuje bibliografii a bibliografické odkazy
We investigated non-invasively cardiac contractility and autonomic nervous activity during presyncopal orthostatic stress induced in healthy humans. A graded orthostatic stress (GOS) paradigm, consisting of head-up tilt (HUT) combined with lower body negative pressure (LBNP) of increasing magnitude, was used to reach a presyncopal end-point in 15 healthy adults. Continuous beat-to-beat hemodynamic and autonomic parameters were recorded. From supine control (C1) to presyncope (PS), total peripheral resistance index (TPRI) decreased from 2300±500 to 1910±320 dyne*s*m²/cm^5 (p=0.004), index of contractility (IC) from 59±14 to 27±6 1000/s (p<0.0001), left ventricular working index (LVWI) from 5.2±1.3 vs. 3.6±0.6 mmHg*L/(min*m²) (p=0.0001) and acceleration index (ACI) from 65±18 vs. 54±15 100/s² (p=0.04). Low frequency variation of diastolic blood pressure (LFnudBP) increased from 51±14 to 67±11 % (p=0.0006) and of systolic blood pressure (LFnusBP) from 50±6 vs. 67±8 % (p<0.0001). High frequency variation of RR-interval (HFms²RRI) decreased from 385±320 to 38±43 ms² (p=0.001). From late GOS (G3) to PS, TPRI decreased from 2540±640 to 1910±320 dyne*s*m²/cm^5 (p=0.003), IC from 35±6 to 27±6 1000/s (p=0.003), LVWI from 4.6±0.9 to 3.6±0.6 mmHg*L/(min/m²) (p=0.003), LFnusBP from 71±8 to 67±8 % (p=0.03), LFmmHg²dBP from 6.6±4.0 to 4.8±2.9 mmHg² (p=0.0001), LFmmHg²sBP from 9.7±7.8 to 7.4±4.8 mmHg² (p=0.01). HFnuRRI increased from 19±8 to 28±13 % (p=0.008). Myocardial contractility indices and parameters of sympathetic activity were reduced in the presyncopal state, while parasympathic activity was increased. This suggests a decrease in cardiac contractility during orthostatically induced presyncope in healthy subjects., E. K. Grasser, N. Goswami, H. Hinghofer-Szalkay., and Obsahuje seznam literatury
The development of neurogenic pulmonary edema (NPE) can be elicited by an immediate epidural balloon compression of the thoracic spinal cord. To evaluate whether a slower balloon inflation could prevent NPE development, we examined the extent of NPE in animals lesioned with a rapid (5 μl - 5 μl - 5 μl) or slow rate (3 μl - 2 μl - 2 μl - 2 μl - 2 μl - 2 μl - 2 μl) of balloon inflation. These groups were compared with the NPE model (immediate inflation to 15 μl) and with healthy controls. Slow balloon inflation prevented NPE development, whereas the pulmonary index and histology revealed a massive pulmonary edema in the group with a rapid rate of balloon inflation. Pulmonary edema was preceded by a considerable decrease in heart rate during the inflation procedure. Moreover, rapid inflation of balloon in spinal channel to either 5 μl or 10 μl did not cause NPE. Thus, a slow rate of balloon inflation in the thoracic epidural space prevents the development of neurogenic pulmonary edema, most likely due to the better adaptation of the organism to acute circulatory changes (rapid elevation of systemic blood pressure accompanied by profound heart rate reduction) during the longer balloon inflation period. It should be noted that spinal cord transection at the same level did not cause neurogenic pulmonary edema., J. Šedý ... [et al.]., and Obsahuje seznam literatury
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