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Hypertensive Group (hypertensive + group)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Tissue kallikrein activity in pregnancy

AUSTRALIAN AND NEW ZEALAND JOURNAL OF OBSTETRICS AND GYNAECOLOGY, Issue 4 2000
S M Khedun
Summary: To determine tissue kallikrein (TK) activity in black African women with hypertensive disorders of pregnancy; 140 women were recruited and divided into the following groups: group A , 35 preeclamptic women, group B , 35 mild to moderate hypertensive pregnant women and group C , 35 normotensive pregnant women, and group D , 35 normotensive non-pregnant healthy women. The activity of tissue kallikrein was determined from a random untimed urine sample using a selective, synthetic chro-mogenic tripeptide substrate having the sequence H-D-Val-Leu-Arg-pNA (S-2266). Urinary sodium and potassium levels was determined by flame photometry. Tissue kallikrein activity was decreased in women with preeclampsia (1.54 ± 0.95 vs 3.05 ± 0.83 ngTK/,g protein; p < 0.0001) and mild to moderate hypertensive group (2.03 ± 0.76 vs 3.05 ± 0.83 ngTK/,g protein; p < 0.0001) compared with normotensive pregnant women. There was also a significant difference in tissue kallikrein activity between the pregnancy groups (1.54 ± 0.95 vs 2.03 ± 0.76 ngTK/,g protein; p < 0.001). No difference in tissue kallikrein activity was observed between normotensive pregnant and normotensive non-pregnant healthy women (3.05 ± 0.83 vs 3.14 ± 0.88 ngTK/,g protein; p = 0.51). There was no difference in the excretion of urinary sodium and potassium in pregnancy groups compared to normotensive pregnant group. Tissue kallikrein activity is decreased in hypertensive disorders of pregnancy. [source]

STUDY OF THE RELATIONSHIP BETWEEN THE KAZAKH'S LIFESTYLE AND GENETIC FACTORS, AND HYPERTENSION, IN THE NORTH-WEST OF CHINA

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 2007
NF Li
SUMMARY 1We investigated the relationship between genetic and environmental factors in hypertensive people living in the Xinjiang Uygur Autonomous Region of China. 2Body mass index, alcohol intake, serum total cholesterol, low-density lipoprotein-cholesterol and triglyceride level in the hypertensive group were significantly higher than corresponding values in the normal group. 3Angiotensinogen gene polymorphisms and related haplotype H6 and H9 were strongly associated with essential hypertension. The b2 -adrenergic receptor gene was associated with lipid disorders in Kazakhs in Xinjiang. 4The results suggest that both genetic and environmental factors play an important role in the development of hypertension in Kazakhs in Xinjiang. [source]

Neural control of the renal vasculature in angiotensin II-induced hypertension

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 10 2002
Rohit Ramchandra
Summary 1.,Chronic administration of angiotensin (Ang) II causes an increase in blood pressure via a multitude of actions, including direct vasoconstriction, hypertrophy and increased sympathetic nerve activity. In the present study, we assessed whether the hypertension resulting from chronic AngII alters the ability of the renal vasculature to respond to sympathetic activity. 2.,Angiotensin II was administered for 7 weeks via an osmotic minipump at a dose of 50 ng/kg per min, i.v., to a group of six rabbits. Blood pressure, measured at 0, 1, 2 and 6 weeks after insertion of the pump, increased from 76 ± 2 to 104 ± 6 mmHg at the end of 6 weeks, without any significant change in heart rate. The blood pressure in the control group remained constant at 76 ± 2 mmHg. 3.,After 7 weeks, rabbits were anaesthetized and the renal nerves were stimulated at 0.5, 1, 1.5, 2, 3, 5 or 8 Hz for 3 min at their supramaximal voltage (5.5 ± 1.0 V in the normotensive group and 6.5 ± 1.5 V in the hypertensive group) while the renal blood flow (RBF) response was recorded. Under anaesthesia, there was no difference in mean arterial pressure between the normotensive and hypertensive animals (77 ± 2 and 80 ± 7 mmHg, respectively). The resting RBF under these conditions was not significantly different in the hypertensive group (30 ± 4 vs 26 ± 5 mL/min in the normotensive vs hypertensive group, respectively). 4.,Stimulation at increasing frequencies was associated with increasing reductions in RBF (e.g. 36 ± 8% at 2 Hz in normotensive rabbits and 48 ± 7% at 2 Hz in hypertensive rabbits). However, there were no significant differences between RBF responses in normotensive and hypertensive rabbits. 5.,We conclude that hypertension associated with chronic AngII administration does not alter the response in RBF to electrical stimulation of the nerves. [source]

Adaptative or maladaptative hypertrophy, different spatial distribution of myocardial contraction

CLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 1 2010
Francesco Cappelli
Summary Background:, Left ventricular hypertrophy (LVH) may be an adaptative remodelling process induced by physical training, or result from pathological stimuli. We hypothesized that different LVH aetiology could lead to dissimilar spatial distribution left ventricular (LV) contraction, and compared different components of LV contraction using 2-dimensional (2-D) speckle tracking derived strain in subjects with adaptative hypertrophy (endurance athletes), maladaptative hypertrophy (hypertensive patients) and healthy controls. Method:, We enrolled 22 patients with essential hypertension, 50 endurance athletes and 24 healthy controls. All subjects underwent traditional echocardiography and 2-D strain evaluation of LV longitudinal, circumferential and radial function. LV basal and apical rotation and their net difference, defined as LV torsion, were evaluated. Results:, LV wall thicknesses, LV mass and left atrium diameter were comparable between hypertensive group and athletes. LV longitudinal strain was reduced only in hypertensive patients (P < 0·05). LV apex circumferential strain was higher in hypertensive patients than in other groups (P < 0·001), LV basal circumferential strain, although slightly increased, did not reach significant difference. Hypertensive patients showed significantly increased rotation and torsion (P < 0·001), while no differences were observed between athletes and control. Conclusion:, In patients with pathological LVH, LV longitudinal strain was reduced, while circumferential deformation and torsion were increased. No differences were observed in LV contractile function between subjects with adaptative LVH and controls. In pathological LVH, increasing torsion could be considered a compensatory mechanism to counterbalance contraction and relaxation abnormalities to maintain a normal LV output. [source]