Search PubMed⌕ Search

Biomedical subjects

J Levenson

Publications and source records attributed to J Levenson.

At least 91 records · Page 5Linked to original sources
PubMed1993

Longitudinal associations between plasma viscosity and cardiovascular risk factors in a middle-aged French population.

A recent prospective study has suggested that increased plasma viscosity may be associated with higher risk of coronary heart disease. A longitudinal approach was used to investigate associations between plasma viscosity and conventional risk factors in an apparently healthy French population aged 45-56 years (637 men and 431 women) over a 2-year follow-up period. In univariate analysis, change in plasma viscosity was significantly related to changes in smoking status, systolic and diastolic blood pressure, gamma glutamyl transferase (gamma GT), body mass index and triglycerides only in men, and to changes in total cholesterol, low-density lipoprotein (LDL) cholesterol and apolipoprotein (apo) B in both sexes. Change in plasma viscosity was also significantly associated with changes in fibrinogen and hemoglobin levels in both sexes. No association was found with age, high-density lipoprotein (HDL) cholesterol or apo A1 in both sexes, or with changes in smoking and menopausal status in women. In multiple stepwise regression analysis, independent determinants of change in plasma viscosity were changes in smoking status, systolic blood pressure, gamma GT, total cholesterol, fibrinogen and hemoglobin in men, and changes in fibrinogen and apo B in women. These results strengthen the hypothesis that increased plasma viscosity may be one of the mechanisms linking conventional risk factors to the risk of cardiovascular disease and suggest that its decrease may be obtained by appropriate life-style changes.

Age Factors↗
PubMed1993

Intrinsic effect of antihypertensive treatment with isradipine and metoprolol on large artery geometric and elastic properties.

The effects of isradipine and metoprolol were studied on the brachial arteries of two groups of 14 patients with hypertension, 90 minutes after the first dose and after 3 months of treatment. Diameter (pulsed Doppler) and compliance (pulse-wave velocity) were measured and calculated in isobaric conditions by way of a model that allowed discrimination of the active intrinsic drug action. Isradipine increased measured and isobaric diameter during short-term (p < 0.05) and long-term administration (p < 0.05), whereas metoprolol did not change it. Active diameter effects were different between drugs during short-term administration (p < 0.05). Isaradipine increased measured and isobaric compliance during short-term (p < 0.05) and long-term administration (p < 0.05). Short-term administration of metoprolol decreased measured compliance (p < 0.01). Metoprolol decreased isobaric compliance during short-term (p < 0.01) and long-term (p < 0.05) administration. Active compliance effects were different between drugs during short- and long-term administration (p < 0.01). These arterial intrinsic drug effects, independent of the pressure-lowering influence, suggested different mechanisms, consisting of a large artery smooth muscle relaxation for isradipine and an isometric arterial constriction for metoprolol.

Adult↗
PubMed1993

Preventive effect of chronic converting enzyme inhibition on aortic stiffening induced by renovascular hypertension in conscious dogs.

OBJECTIVE: The aim was to assess the influence of the renin-angiotensin system on the geometrical and elastic properties of the aorta in conscious dogs, using a model of renovascular hypertension, and to examine the effects of inhibition of the system by the angiotensin converting enzyme inhibitor spirapril. METHODS: The aortic elastic behaviour in response to renovascular hypertension was studied in 15 conscious dogs instrumented with a pressure microtransducer and a pair of ultrasonic diameter dimension gauges in the upper descending thoracic aorta. Renovascular hypertension was induced by surgical occlusion of one renal artery and stenosis of the other. One day after renal surgery, dogs were randomly assigned to two groups receiving for two months either the new angiotensin converting enzyme inhibitor spirapril (n = 8) or a placebo capsule (n = 7). The two groups of dogs were compared to a control group of normotensive dogs (n = 7). After two months of treatment the elastic properties of the aorta were studied by computation of the beat to beat pressure-diameter hysteresis loops obtained during transient increase of pressure induced by bolus doses of angiotensin. The aortic pressure-diameter (P-D) relationship, obtained over a wide range, was fitted by an exponential fit (P = alpha.e beta D), where beta is the stiffness index. A decomposition of the P-D curve according to a biphasic model of the parallel arrangement of elastin and collagen enabled two pressure-diameter elastic moduli to be obtained, one representing the resistance to stretch at low pressure levels (elastic fibres and smooth muscle), and the other representing the resistance to stretch at the highest pressures (collagen fibres). RESULTS: The pressure-diameter curve of the placebo group was shifted to the left compared to the curves of the control and spirapril groups, showing that renovascular hypertension was associated with isobaric reduction of aortic diameter. The stiffness index beta was higher (p < 0.05) in the placebo group [0.605(SD 0.304) mm-1] than in either the control group [0.362(0.126) mm-1] or the spirapril group [0.348(0.083) mm-1], suggesting that renovascular hypertension was associated with aortic stiffening. The biphasic analysis showed that the collagen pressure-diameter elastic modulus was unaffected by spirapril, whereas the elastin pressure-diameter elastic modulus was significantly reduced by converting enzyme inhibitor with respect to the placebo (p < 0.05). CONCLUSIONS: Chronic converting enzyme inhibition by spirapril prevents the isobaric aortic diameter reduction induced by renovascular hypertension in conscious dogs and decreases aortic stiffness, in particular by changing the elastic behaviour of the elastin fibres rather than of the collagen fibres.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1993

In vivo shear flow and erythrocyte membrane fluidity in hypertensive patients.

1. To evaluate the response of red blood cells subjected to the shear flow in hypertension, the relationships between wall shear phenomena determined in vivo in the brachial artery of hypertensive patients and the modifications of the membrane dynamics measured in vitro in erythrocyte ghosts of 32 patients were investigated. 2. Two fluorescent probes, diphenylhexatriene (DPH) and its trimethylamino-derivative (TMA-DPH), localized respectively in the lipid membrane core and at the lipid-water interface, were used. 3. Shear rate, shear stress and blood velocity were positively correlated with TMA-DPH anisotropy (P = 0.015, 0.005 and 0.026, respectively), but not with that of DPH. This indicates that wall shear forces were associated with the microviscosity of the outer part of the cell membrane. 4. The changes in wall shear forces and erythrocyte membrane microviscosity probed by TMA-DPH or DPH were observed to vary in parallel under nitrendipine therapy. 5. These results suggest that in vivo shear forces participate in the control of erythrocyte membrane fluidity or that erythrocytes adapt their membrane properties to blood flow conditions.

Antihypertensive Agents↗
PubMed1993

Evidence for in vivo carotid and femoral wall thickening in human hypertension. Groupe de Prévention Cardio-vasculaire en Médecine du Travail.

Little is known of the in vivo structural changes of large arteries in uncomplicated hypertension. Therefore, we measured the intima-media thickness and lumen diameter of common carotid and femoral arteries by a computerized ultrasonographic technique in 25 normotensive and 25 never treated hypertensive men of similar age (from 25 to 72 years). The intraobserver variability of carotid and femoral wall thicknesses was 4.3% and 5.6%, respectively. Moreover, an in vitro study of 13 human arterial segments removed at autopsy demonstrated a strong correlation (r = .989, P < .001) between computerized ultrasonic and histological intima-media thickness measurements. Compared with control subjects, hypertensive patients had similar arterial diameters but higher carotid and femoral intima-media thicknesses (P < .001) as well as higher ratios of carotid and femoral intima-media thickness to lumen (P < .001, P < .01). The carotid thickness was correlated with age in control subjects (r = .48, P < .05) but not in hypertensive patients. The femoral thickness was correlated with age both in control subjects (r = .55, P < .01) and in hypertensive patients (r = .46, P < .05). Thus, carotid and femoral arterial walls of hypertensive patients were thickened. This thickening was not due to age, although aging also thickened both vessels in control subjects and the femoral artery only in hypertensive patients. Such a wall thickening associated with a normal diameter provides direct evidence of vascular growth and represents a new target to monitor noninvasively in vivo for large artery changes in human hypertension.

Adult↗
PubMed1993

Assessment of smooth muscle contribution to descending thoracic aortic elastic mechanics in conscious dogs.

Early investigators found contradictory evidence that vascular smooth muscle activation reduces the elastic modulus of the arterial wall under isotonic conditions but increases it under isometric conditions, concomitant with increased pulse-wave velocity. We examined the individual contributions of aortic constituents to the elastic modulus of the aortic wall to determine if isobaric analysis produces an accurate assessment of vascular smooth muscle activation. We used a modified Maxwell model assuming an incremental elastic modulus (Einc) composed of the elastic modulus of elastin fibers (EE), the elastic modulus of collagen fibers (EC) affected by the fraction of collagen fibers (fC) recruited to support wall stress, and the elastic modulus of the vascular smooth muscle (ESM) according to the following formula: Einc = EE+EC x fC+ESM.Einc was assessed in eight conscious dogs using descending thoracic aortic pressure (microtransducer) and diameter (sonomicrometry) measurements. Stress-strain relations in the control state and during activation of smooth muscle by continuous administration of phenylephrine (5 micrograms.kg-1 x min-1) were obtained by transient occlusions of the descending aorta and inferior vena cava. Results were as follows: EE was 4.99 +/- 1.58 x 10(6) dynes/cm2 (mean +/- SD), and EC was 965.8 +/- 399.8 x 10(6) dynes/cm2, assessed during the control state. Phenylephrine administration increased the theoretical pulse-wave velocity (Moens-Korteweg equation) from 5.25 +/- 1.03 m/s during the control state to 7.57 +/- 2.53 m/s (P < .005). Active muscle exhibited a unimodal stress-strain curve with a maximum stress of 0.949 +/- 0.57 x 10(6) dynes/cm2 at a corresponding strain value of 1.299 +/- 0.083. The maximum value observed corresponded, on the pressure-diameter curve of the active artery, to a pressure of 234.28 +/- 46.6 mm Hg and a diameter of 17.94 +/- 1.6 mm. The maximum ESM derived from the stress-strain relation of the active muscle was 8.345 +/- 7.56 x 10(6) dynes/cm2 at a strain value of 1.283 +/- 0.079. This point was located at 208.01 +/- 40.8 mm Hg and 17.73 +/- 1.41 mm on the active pressure-diameter curve. During activation of vascular smooth muscle, Einc decreased (P < .05) when plotted against internal pressure but increased (P < .05) when plotted against strain, over the operative range.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

Early detection of subclinical atherosclerosis in asymptomatic subjects at high risk for cardiovascular disease.

Subclinical atherosclerosis can be non-invasively detected via calcifications, thickening and stiffening of arteries. Coronary calcifications seen with ultrafast computed tomography are frequent in hypertension or hypercholesterolemia and synonymous of coronary atherosis but not of coronary stenosis. Wall thickening detectable by extracoronary ultrasonography may be characterized by an intimamedia thickening shown in hypertension or by a focalized plaque whose the presence in the aortic or femoral level seem influenced by systolic pressure. Extracoronary wall thickening may be an aid in the diagnosis of coronary atherosclerosis, a predictor of coronary event, and a therapeutic target. Wall stiffening, which reflects sclerosis, is detected by pulse wave velocity. Its increase in hypertension may be an indicator of atherosclerosis and can be reversed by certain antihypertensive agents. Clinical care of at risk individuals might profit from subclinical atherosclerosis which adds objectivity and sensitivity in the individualization of risk and the decision to treat.

Arteriosclerosis↗
PubMed1993

[Estradiol and progesterone physiological substitution effects on the hemodynamics of the humeral artery in women with inactive ovaries].

To determine the effects of female hormones on peripheral vasculature we studied the brachial artery circulation. Nine young women (27-37 yrs) having inactive ovaries received transdermal estradiol (E2) (0.1-0.4 mg/d) and vaginal progesterone (P) (300 mg/d) to duplicate the menstrual cycle levels of E2 and P. Brachial artery diameter, blood velocity and flow were measured by bidimensional pulsed Doppler in basal conditions, and during hand exclusion by a cuff inflated at suprasystolic pressure. Vascular resistance was calculated by the ratio of mean blood pressure over mean flow. Measurements were obtained before hormonotherapy (d0), on day 14 (d14, after E2), and on day 28 (d28, after E2 and P). The increase of brachial artery diameter began at d14 (3.73 +/- 0.12 mm, vs 3.66 +/- 0.11 mm; NS) to become significant at d28 (3.91 +/- 0.10 mm, p < 0.05). Blood velocity and flow increased at d28 (4.78 +/- 0.55 cm/s, vs 3.55 +/- 0.65 cm/s; P < 0.05 and 35.2 +/- 5.2 ml/mn vs 22.2 +/- 3.6 ml/mn, P < 0.05 respectively). No change was noted in mean blood pressure. The decrease of resistance began at d14, in order to be significant at d28 (158 +/- 17 mmHg/ml/s at d0 vs 263 +/- 31 mmHg/ml/s at d28; P < 0.05). Brachial vasoconstriction during hand exclusion, in response to low flow state disappeared at d14 with estradiol. In conclusion, in women deprived of ovarian function, physiological E2 and P replacement vasodilates small and large arteries, whereas E2 alone attenuates the large artery vasoconstriction in acute response to low flow state.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Cutaneous↗
PubMed1992

Hypercholesterolaemia alters arterial and blood factors related to atherosclerosis in hypertension.

To evaluate the influence of hypercholesterolaemia on arterial and blood factors related to cardiovascular disease in hypertension, 20 normocholesterolaemic and 31 hypercholesterolaemic hypertensive patients underwent determinations of whole blood filterability (WBF), plasma fibrinogen concentration (PF) and aortic pulse wave velocity (PWV). Both of the groups had similar age, body mass index, cumulative smoking dose and blood pressure. Hypercholesterolaemics had lower WBF (P less than 0.02), higher PF (P less than 0.02) and higher PWV (P less than 0.01) than normocholesterolaemics. In the whole population WBF correlated with age (P less than 0.005), mean blood pressure (P less than 0.01), total cholesterol (P less than 0.05) and plasma fibrinogen (P less than 0.01). However, in a multivariate analysis where age and pressure were controlled as variables, only the association between WBF and PF remained significant (P less than 0.001). Thus, the higher fibrinogen affects whole blood filterability in hypercholesterolaemic hypertensive patients. In the whole population PWV correlated positively with HDL cholesterol (P less than 0.01) and age (P less than 0.001) and the association with HDL cholesterol remained significant in a multivariate analysis (P less than 0.001) where age was controlled. The effect of ageing on arterial rigidity seems to be similar in both hypertensive groups as deduced from the identical regression slopes relating pulse wave velocity to age. So in hypertension with high cholesterol, arterial rigidity was increased without changes in arterial stiffening with age.

Aorta↗
PubMed1992

Biochemical and functional alterations associated with hypercholesterolemia in platelets from hypertensive patients.

Hypercholesterolemia and hypertension are two of the major risk factors associated with increased atherosclerotic vascular disease. An abnormal platelet function is one of the mechanisms proposed to participate in atherogenesis. This study was undertaken to find out whether hypercholesterolemia in hypertensive patients can change platelet lipid composition and reactivity. Twenty-nine untreated hypertensive patients were distributed into 3 age, body mass index and blood pressure-matched groups according to their plasma cholesterol levels (normal, borderline or elevated, group NC, BC and HC respectively). Their platelet lipid composition, cytosolic Ca2+ concentration, cyclic AMP content and aggregating response to ADP and collagen were determined. Platelet from group HC patients were characterized by reduced cyclic AMP content (evaluated in the presence and absence of a platelet phosphodiesterase inhibitor) and aggregating responses to ADP and collagen, increased palmitic acid content and decreased arachidonic, eicosapentaenoic and docosatetraenoic and pentaenoic acid content, resulting in a lowered polyunsaturated to saturated fatty acid ratio (P less than 0.001). In contrast, platelet cytosolic Ca2+ concentration, DPH steady-state anisotropy and cholesterol to phospholipid molar ratio were not significantly changed. This indicates that hypercholesterolemia is accompanied in hypertensive patients by marked changes in platelet fatty acid composition, cyclic AMP content and response to aggregating agents. These changes, which clearly differ from those induced by in vitro cholesterol loading, could reflect not only the balance between LDL and HDL stimulation but also an adaptation to hemodynamic perturbations.

Adenosine Diphosphate↗
PubMed1992

Comparative effects of diabetes mellitus and hypertension on physical properties of human large arteries.

OBJECTIVES: The effects of hypertension and diabetes on the physical properties of large arteries were compared in men. BACKGROUND: Although these two diseases are linked to vascular stiffening, no study has analyzed whether the arterial rigidity in diabetes is as substantial as in hypertension. METHODS: Noninvasive measurements of brachial artery mean pressure, diameter (pulsed Doppler study) and compliance (pulse wave velocity) were obtained in 29 men: 11 control subjects, 9 hypertensive nondiabetic patients and 9 diabetic normotensive patients. Individual diameter- and compliance-pressure curves extrapolated from the measured diameter and mean pressure point with a logarithmic elastic model permitted calculation of isobaric diameter and compliance at the same pressure in each subject. RESULTS: Compared with control subjects, hypertensive patients had a larger brachial artery measured diameter and isobaric diameter (p < 0.01) and lower measured and isobaric compliance (p < 0.001, p < 0.01). Compared with control subjects, diabetic patients had lower measured and isobaric compliance (p < 0.01). Comparison of diabetic and hypertensive patients showed that measured diameter and isobaric diameter were decreased in the former (p < 0.01). In the control and hypertensive groups, mean pressure correlated positively with measured diameter and isobaric diameter (p < 0.01) and negatively with measured and isobaric compliance (p < 0.001 and p < 0.01, respectively). In the control and diabetic groups, fasting glucose correlated negatively with measured and isobaric compliance (p < 0.01, p < 0.05). CONCLUSIONS: Intrinsic alterations of the large artery independent of a stretching pressure effect reduce arterial elasticity similarly in those with hypertension or diabetes. The loss of compliance is related to the chronic elevation of blood pressure in hypertension and to that of glycemia in diabetes and is associated with a relative large artery vasoconstriction in diabetic patients as compared with patients with hypertension.

Adult↗
PubMed1992

Diuretics and arteriolar resistance and arterial compliance in human hypertension.

Differences exist between short- and long-term haemodynamic effects of diuretics. In the short term, plasma volume depletion is accompanied by increased peripheral vascular resistance and decreased cardiac output. In the long term cardiac output returns toward normal, peripheral resistance falls to below pretreatment values and blood volume remains lower than before therapy. This long-term decrease in volume may contribute to the chronic antihypertensive effects of diuretics. Many studies have reported that arterial compliance is increased after antihypertensive drug administration. However, it is important to known whether such action is a primary pharmacological effect or mediated by the reduction in blood pressure. Two different methods using pulse wave velocity measurements have been applied to determine the pressure-dependence of compliance before and after thiazide administration. In the first method, blood pressure was controlled as a variable by changing transmural pressure of the forearm encased in a rigid plastic tube. In the other method arterial compliance in the brachial artery was evaluated using a simple non-linear arterial model. Both methods demonstrated that the decrease in blood pressure with thiazide therapy was associated with increased arterial compliance. However, by measuring arterial compliance at the same pressure, its isobaric values were found to be unchanged. The implication is that the increase in compliance of the peripheral artery observed with diuretics is due to the decline in blood pressure rather than to a change in the intrinsic properties of the arterial wall.

Arterioles↗
PubMed1992

Active and passive effects of antihypertensive drugs on large artery diameter and elasticity in human essential hypertension.

The effects of antihypertensive drugs on the large arteries consist of two parts: the passive effect due to the change in pressure and the active effect, the drug action per se. This study proposes a method of dissociating the passive effect from the active effect. The diameter of the arterial artery was determined by the pulsed Doppler method and the pulse wave velocity of the brachioradial artery by mecanography. Arterial compliance was calculated by the Bramwell-Hill formula. Active and passive effects were determined by a logarithmic pressure-diameter model. This model was supported by in situ direct measurements of blood pressure and diameter in a segment of the femoral artery in dogs. Six drugs, cadralazine, ketanserin, medroxalol, nitrendipine, captopril, and isosorbide dinitrate, administered orally, were tested in 70 essential hypertensive patients. For all drugs, the pressure reduction induced a passive decrease in arterial diameter (p less than 0.02 to p less than 0.01). Cadralazine actively decreased arterial diameter (p less than 0.01), ketanserin had no active effect on diameter, and medroxalol, nitrendipine, captopril, and isosorbide dinitrate actively increased arterial diameter (p less than 0.05, p less than 0.01, p less than 0.01, and p less than 0.01, respectively). For all drugs, the pressure reduction also induced a passive increase in arterial compliance (p less than 0.05 to p less than 0.01). However, only nitrendipine, captopril, and isosorbide dinitrate actively increased arterial compliance (p less than 0.01, p less than 0.05, and p less than 0.01, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Serum Lp(a) as a discriminant marker of early atherosclerotic plaque at three extracoronary sites in hypercholesterolemic men. The PCVMETRA Group.

To investigate the role of lipoprotein (a) (Lp[a]) as an atherogenic condition related to hypercholesterolemia, we studied the serum concentration of Lp(a) as measured by immunonephelometry in relation to the presence of asymptomatic echographic plaques in the peripheral arteries of 103 untreated hypercholesterolemic, normotensive, middle-aged men. Plaque was found at carotid, aortic, and femoral sites in 36%, 51%, and 53% of subjects, respectively. The Lp(a) level was higher in the group with carotid plaques than in the group without (0.29 +/- 0.20 versus 0.17 +/- 0.14 g/l, p < 0.01), not significantly higher in the group with aortics plaque than in the group without (0.24 +/- 0.19 versus 0.19 +/- 0.16 g/l), and not different between groups with and without femoral plaques (0.21 +/- 0.18 versus 0.22 +/- 0.17 g/l). A logistic regression analysis confirmed that Lp(a) was associated with carotid plaques (p = 0.004), independent of other risk factors. However, in patients with low density lipoprotein cholesterol values above the group median value (4.7 mmol/l), Lp(a) was associated not only with carotid plaques (p < 0.01) but also with aortic plaques (p < 0.05), as well as with the number of diseased sites (p = 0.02). In contrast, in patients with low density lipoprotein cholesterol levels below or equal to 4.7 mmol/l, Lp(a) only remained associated with carotid plaques (p < 0.05). Thus, in symptom-free, hypercholesterolemic men, early atherosclerosis was influenced by serum Lp(a), particularly in the carotid arteries, as well as by the presence of a higher level of low density lipoprotein cholesterol.

Adult↗
PubMed1992

Coronary calcification and its relation to extracoronary atherosclerosis in asymptomatic hypercholesterolemic men. The PCV METRA Group.

BACKGROUND: The prevalence of coronary calcifications and extracoronary plaques was studied in patients with asymptomatic hypercholesterolemia. METHODS AND RESULTS: Ultrafast computed tomography for coronary calcification (presence or absence: calcium score) and echographic assessment of carotid, aortic, and femoral plaques were performed in 111 hypercholesterolemic men: 65% had coronary calcification, 72% had extracoronary plaque. The two lesions were associated as: 1) compared with subjects without coronary calcification, those with calcification had a higher prevalence of aortic (p less than 0.05) and femoral (p less than 0.01) plaque and of two diseased sites (p less than 0.05); 2) the prevalence of coronary calcification was higher in the presence than in the absence of aortic (p less than 0.05) or femoral (p less than 0.01) plaque and higher in two (p less than 0.01) and three diseased (p less than 0.05) sites than in no diseased site; 3) the calcium score was higher in the presence than in the absence of carotid (p less than 0.05), aortic (p less than 0.05), or femoral (p less than 0.001) plaque, higher in two (p less than 0.001) and three diseased (p less than 0.05) sites than in no diseased sites, and higher in two (p less than 0.01) than in one diseased site; and 4) the calcium score correlated with femoral plaque (p less than 0.001). Overall, the presence of two or three diseased extracoronary sites versus no or one diseased site showed a power of 78% for predicting coronary calcification. Coronary calcium score correlated with age (p less than 0.01) and triglycerides (p less than 0.05). CONCLUSIONS: The close relation between coronary calcium and extracoronary plaques suggests that echography of extracoronary vessels could aid in the screening of coronary atherosclerosis in high-risk, asymptomatic individuals.

Adult↗
PubMed1992

Control of the erythrocyte free Ca2+ concentration in essential hypertension.

Since Ca2+ ions seem to directly participate in the control of erythrocyte membrane structure and deformability and because cell Ca2+ metabolism has been repeatedly proposed to be modified in hypertension, the intracellular calcium ion concentration ([Ca2+]i) was investigated in red blood cells from hypertensive and normotensive subjects. [Ca2+]i was measured by using the fluorescent Ca2+ chelator fura-2. Red blood cell [Ca2+]i was increased in hypertensive compared with normotensive subjects in the whole population and further increased when hypertensive were compared with age-matched normotensive subjects. An inverse relation between age and [Ca2+]i was observed when calculated with blood pressure adjusted. In hypertensive patients, high [Ca2+]i values were associated with a reduced erythrocyte deformability. The initial rate of 45Ca2+ uptake did not differ between the two blood pressure groups. Similarly, when the extracellular Ca2+ concentration was elevated from 1 to 2 mmol/l, [Ca2+]i increased by 16 +/- 4% (p less than 0.03) in red blood cells from both groups, thus maintaining a significant difference between hypertensive and normotensive subjects. Under these conditions, the addition of 10(-7) mol/l nicardipine, a dihydropyridine Ca2+ antagonist, decreased [Ca2+]i by 15 +/- 4% (p less than 0.05) and 7 +/- 5% in erythrocytes from hypertensive and normotensive subjects, respectively, thereby reducing the difference in [Ca2+]i observed between these two groups. This nicardipine effect was positively correlated to the initial [Ca2+]i. In the presence of 5 mumol/l W7, a calmodulin antagonist, [Ca2+]i increased significantly only in erythrocytes from hypertensive patients (26 +/- 6%, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium↗
PubMed1992

Increase in erythrocyte disaggregation shear stress in hypertension.

The aggregation and disaggregation behaviors of red blood cells were investigated in 17 normotensive and 21 hypertensive subjects with a laser reflectometry technique, and simultaneous measurements were taken of blood viscosity with a coaxial viscometer. Increased red blood cell aggregation (26%, p less than 0.001) and disaggregation shear rate (20%, p less than 0.01) and shear stress (18%, p less than 0.01) were observed in hypertensive subjects when compared with normotensive subjects. Similar elevations in hypertensive subjects were found when the hematocrit was adjusted to 40%. Variation of red blood cell concentration caused the red blood cell disaggregation shear rate to change in an opposite direction but did not modify red blood cell aggregability and disaggregation shear stress. The increase of the reversible aggregation of red blood cells was associated with higher fibrinogen and plasma protein concentrations in hypertension. An increase in red blood cell aggregability and in the shear resistance of red blood cell aggregates may play a role in the development of the cardiovascular complication in hypertension. The quantification of red blood cell disaggregation shear stress, which represents the hydrodynamic force required to disperse the aggregates, may provide a useful parameter for clinical investigations.

Adult↗