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Effect of long-term intake of isoleucine-proline-proline (IPP) and valine-proline-- proline (VPP), or a sour milk product containing these peptides on development of hypertension was investigated in spontaneously hypertensive rats (SHR). Six-week-old SHR were given: 1) water (control group), 2) IPP and VPP dissolved in water (peptide group) or 3) sour milk containing IPP and VPP (sour milk group) for 12 weeks. Systolic blood pressure (SBP) was measured by tail-cuff method. Development of hypertension was attenuated in the groups receiving tripeptides or sour milk as compared to the control group. At the end of treatment period, SBP was 176 ± 1 mmHg in sour milk group, 181 ± 2 mmHg in peptide group, and 193 ± 1 mmHg in control group (P < 0.001). After treatment withdrawal, SBP rose gradually reaching the level of control group within four weeks’ follow-up. In functional bioassay of ACE inhibitory activity, effect of the tripeptides on angiotensin I or angiotensin II-induced contraction in rat mesenteric arteries was evaluated. IPP inhibited the angiotensin I -induced contraction, whereas the angiotensin II-induced contraction remained unaltered. In conclusion, long-term intake of IPP and VPP, or a sour milk containing these tripeptides attenuated the development of hypertension in SHR. One possible mechanism underlying this effect is ACE inhibition.
Endothelial nitric oxide synthase (eNOS) is known as mediator of endothelium-dependent vasodilatation. The gene encoding this enzyme is regarded as one of the candidate for risk of developing hypertension. The aim of our study was to investigate whether polymorphism in intron 4 (4a/b) of eNOS gene is associated with hypertension. Gene variants were determined by PCR method among 82 healthy, normotensive and 62 hypertensive individuals. In the group of patients with hypertension as compared to the controls higher frequency of 4a4a+4a4b genotypes (45.2% vs 23.5%) and lower frequency of 4b4b genotype (54.8% vs 76.5%) was observed. The data indicate a significant association between presence of 4a allele of eNOS gene and hypertension in studied population.
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.
Atrial natriuretic peptide (ANP) regulates blood pressure mainly through the occupation of the guanylyl cyclase-coupled receptor NPR-A, which requires ATP interaction for maximal activation. This study investigates the effect of extracellular Ca2+ on ATP-mediated regulation of NPR-A-coupled guanylyl cyclase activity in glomerular membranes from Wistar Kyoto (WKY) and spontaneously hypertensive rats (SHR). ATP induced a significant increase in basal and ANP1-28-stimulated guanylyl cyclase activity that was greater in SHR than in WKY. Extracellular Ca2+ inhibited ATP-stimulated guanylyl cyclase activity in a concentration-dependent manner, but did not modify basal and ANP1-28-stimulated guanylyl cyclase activity. In the presence of ATP, NPR-A showed higher affinity for ANP1-28 and lower Bmax. Ca2+ did not modify NPR-A-ANP1-28 binding properties. The different effects of extracellular Ca2+ on ANP1-28- or ATP-mediated guanylyl cyclase activation suggest that these events are differentially regulated. Addition of extracellular Ca2+ induced similar effects in hypertensive and normotensive rats, suggesting that it is not responsible for the elevated cGMP production observed in SHR.
Our previous studies suggested that acylation of the N-terminus of several known B2 antagonists with various kinds of bulky acyl groups consistently improved their antagonistic potency in rat blood pressure assay. On the other hand, our earlier observations also seemed to suggest that the effects of acylation on the contractility of isolated rat uterus depended substantially on the chemical character of the acyl group, as we observed that this modification might either change the range of antagonism or even transform it into agonism. Bearing all this in mind, we decided to synthesize seven new analogues of bradykinin by N-terminal acylation with various acyl groups of a moderately potent B2 antagonist, previously synthesized by Stewart's group, D-Arg-Arg-Pro-Hyp-Gly-Thr-Ser-D-Phe-Thi-Arg. The analogues were tested in vitro for their blood pressure-lowering and uterotonic activities. The modifications either preserved or increased the antagonistic potency in the rat blood pressure test. On the other hand, all seven substituents negatively influenced the interaction with the rat uterine receptors. Our results may be helpful for designing new B2 agonists and antagonists.
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The aim of this study was to evaluate the effects of the stimulation of central cholinergic synapses in the regulation of heat loss in untrained rats during exercise. The animals were separated into two groups (exercise or rest) and tail skin temperature (Ttail), core temperature and blood pressure were measured after injection of 2 µL of 5 x 10-3 M physostigmine (Phy; n = 8) or 0.15 M NaCl solution (Sal; n = 8) into the lateral cerebral ventricle. Blood pressure was recorded by a catheter implanted into the abdominal aorta, Ttail was measured using a thermistor taped to the tail and intraperitoneal temperature (Tb) was recorded by telemetry. During exercise, Phy-treated rats had a higher increase in mean blood pressure (147 ± 4 mmHg Phy vs. 121 ± 3 mmHg Sal; P < 0.001) and higher Ttail (26.4 ± 1.0° C Phy vs. 23.8 ± 0.5° C Sal; P < 0.05) that was closely related to the increase in systolic arterial pressure (r = 0.83; P < 0.001). In addition, Phy injection attenuated the exercise-induced increase in Tb compared with controls without affecting running time. We conclude that the activation of central cholinergic synapses during exercise increases heat dissipation due to the higher increase in blood pressure.
Linkage and association studies suggested the relationship between α-adducin polymorphism (Gly460Trp; rs4961) and genetic susceptibility to salt-sensitivity. However, the currently available results were inconsistent. This study aimed to define quantitatively the association between salt-sensitivity and α-adducin Gly460Trp polymorphism in all published case-control studies. Publications from PubMed and other databases were retrieved. The major inclusion criteria were: (1) case-control design; (2) salt-sensitivity confirmed by sodium loading tests, and (3) the distribution of genotypes given in detail. Seven case-control studies fulfilled the inclusion criteria. In total they involved 820 subjects (454 salt-sensitive and 366 non-salt-sensitive). The meta-analysis shows that Gly460Trp polymorphism in general is not significantly associated with salt-sensitivity [OR (95%CI): 1.40 (0.96,2.04), P = 0.08]. Subgroup analysis showed that the association is statistically significant in Asian people [OR (95%CI): 1.33 (1.06, 1.69), P = 0.02] but not in Caucasian people [OR (95%CI): 1.98 (0.57, 6.92), P = 0.28]. This indicates that blood pressure response to sodium varies between ethnical groups. More studies based on a larger population are required to evaluate further the role of α-adducin Gly460Trp polymorphism in salt-sensitive hypertension.
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