Biomedical subjects

J Levenson

Publications and source records attributed to J Levenson.

At least 127 records · Page 7Linked to original sources

PubMed1990

Effect of beta adrenoceptors and thyroid hormones on velocity and acceleration of peripheral arterial flow in hyperthyroidism.

Brachial artery flow patterns were studied in 10 hyperthyroid and 10 normal subjects. Mean blood velocity and flow were evaluated by pulsed Doppler, and peak systolic acceleration was calculated by computer-assisted digitization of the instantaneous velocity curve. Compared to control subjects, hyperthyroid patients had higher velocity and flow (p less than 0.01, p less than 0.02) and higher peak systolic acceleration (p less than 0.01). In hyperthyroid patients, measurements were repeated after (1) mechanical exclusion of the hand from brachial circulation, (2) short-term beta-blocker treatment and (3) inducement of the euthyroid state. Exclusion of the hand reduced velocity and flow (p less than 0.001) but did not change peak systolic acceleration. Beta blockade induced disparate changes of velocity and flow but reduced peak systolic acceleration (p less than 0.05). In the euthyroid state, decreased blood velocity (p less than 0.01), flow (p less than 0.02) and acceleration (p less than 0.02) were observed. A hyperkinetic arterial circulation consisting of an increase in both velocity and acceleration is thus observable in hyperthyroidism. Hand exclusion showed that velocity seems to be influenced by peripheral factors while beta blockade suggests that acceleration is dependent of beta 1 adrenoceptors. Comparison between euthyroidism and hyperthyroidism indicates that both mean blood velocity and peak systolic acceleration are influenced by thyroid hormones.

Adrenergic beta-Antagonists↗

PubMed1990

A new geometric procedure for in vivo pulsed Doppler evaluation of velocity distribution inside the diametrical section of large arteries in humans.

A new geometric procedure determination of velocity profiles inside large human arteries, such as the brachial and femoral, has been developed. The procedure requires the use of two crystal element Doppler probes and a highly precise micromanipulator with three degrees of freedom. Precise positioning is needed to obtain the required high degree of parallelism between the vessel axis and the plane containing the two crystal elements. Once the appropriate degree of parallelism is achieved, a controlled translation of the probe, perpendicular to the ultrasonic beam plane, allows velocity waveforms to be recorded at sequential radial positions across the measured artery. Velocity profiles obtained with this geometric procedure depended on the type of artery investigated. The profiles measured with the geometric procedure were more symmetrical than those found using the electronic range-gated time system of reception. While the geometric and electronic methods were almost identical in determining the diameter values of the three arteries measured, the geometric procedure enabled greater accuracy for detailed analysis of velocity profiles in the peripheral large arteries in humans. Although the present methodology is not applicable in clinical practice due to prolonged data acquisition time (approximately 45 s) it is expected that future equipment improvements will reduce this time significantly.

Adult↗

PubMed1990

Relation of risk factors for cardiovascular disease to early atherosclerosis detected by ultrasonography in middle-aged normotensive hypercholesterolemic men. PCV Metra Group.

The relations between carotid arteries and/or abdominal aortic plaque and cardiovascular risk factors were investigated by ultrasonography in 161 untreated hypercholesterolemic normotensive men. Of them, 58 had no plaque (NP group), 34 had carotid but not aortic plaque (CP group), 34 had aortic but not carotid plaque (AP group) and 35 had both carotid and aortic plaques (CAP group). Groups significantly differed for age, smoking, blood pressure, and the ratio of total to HDL cholesterol. Age was higher in CAP group than in NP and CP groups and in AP and CP groups than in NP group. Life long smoking dose was higher in CAP group than in CP, AP, and NP groups. Systolic and diastolic pressures were higher in CAP group than in NP group, systolic pressure was higher in CAP group than in CP group, and diastolic pressure was higher in AP group than in CP and NP groups. The ratio of total to HDL cholesterol was higher in CAP group than in AP, CP, and NP groups. Multiple regression analysis showed that carotid plaque was only related to age, while aortic plaque and the number of sites affected by plaque were correlated to age, smoking and diastolic pressure. These findings suggest that in hypercholesterolemia risk factors other than lipids seem to influence arterial plaque and that risk profile differs according to the plaque location.

Adult↗

PubMed1990

Dynamic association between artery shear flow condition and platelet cytosolic free Ca2+ concentration in human hypertension.

1. Blood cells and vascular endothelial cells are subjected to a wide range of haemodynamically generated shear stress forces. In vitro, membrane stretching or shear stress have been observed to activate ion channels and cell metabolism and to facilitate erythrocyte and platelet aggregation. 2. The present study was designed to evaluate the participation of shear stresses in the control of apparent platelet cytosolic free Ca2+ concentration in hypertensive patients. 3. Shear conditions and platelet cytosolic free Ca2+ concentration in vitro were studied after a dynamic perturbation induced by 3 months of double-blind treatment with one of two beta-antagonists, carteolol and atenolol. Brachial artery wall shear rate and stress were estimated by means of a pulsed Doppler velocimeter, and blood viscosity was measured by a co-axial viscometer at a shear rate of 96 s-1. Platelet cytosolic free Ca2+ concentration was simultaneously measured by using the Quin-2 fluorescent chelator. The direct effect of atenolol and carteolol on platelet cytosolic free Ca2+ concentration in vitro was also measured after addition of the beta-blockers to platelet-rich plasma. 4. Atenolol and carteolol decreased blood pressure similarly but their effects on shear rate (P less than 0.02), shear stress (P less than 0.01) and platelet cytosolic free Ca2+ concentration (P less than 0.05) differed after 3 months of therapy. In contrast, neither of the drugs significantly altered platelet cytosolic free Ca2+ concentration, in vitro per se. 5. In the overall population, strong positive correlations existed not only between changes in platelet cytosolic free Ca2+ concentration and those in shear rate (r = 0.81, P less than 0.001) and shear stress (r = 0.83, P less than 0.001), but also between their absolute values, suggesting a possible haemodynamic shear-dependent modulation of transmembrane Ca2+ transport.

Arteries↗

PubMed1990

Effects of muscarinic and beta-adrenergic blockade on the aortic elastic response to epinephrine induced acute hypertension in conscious dogs.

To determine the effects of parasympathetic blockade and beta-blockade on the elastic response of aortic stiffness to vasopressive interventions, we studied 5 unanesthetised adult mongrel dogs by means of a pressure microtransducer and two ultrasonic crystals positioned at opposing sites in the proximal descending thoracic aorta which were used for diameter measurements. Systolic and diastolic changes in pressure and diameter were used to calculate Peterson and incremental elastic moduli. Acute hypertension was induced using infusions of epinephrine during the control period and later propranolol (1.5 mg/kg) plus atropine (0.2 mg/kg). Percent variations of mean aortic diameter were correlated to percent variations in mean aortic pressure in the control period and after autonomic blockade (P less than .001). The slopes of these correlations in the control group were higher than after autonomic blockade (P less than .05). Correlations were also found between Peterson and incremental elastic moduli and mean pressure in the control group and after autonomic blockade (P less than .001). The slopes of the correlations of incremental elastic modulus and Peterson's modulus versus mean aortic pressure were lower in the control group than after blockade (P less than .001). We conclude that in conscious dogs, autonomic blockade with propranolol and atropine decreased the distension and increased the stiffness of the aortic wall in response to acute hypertension mediated by epinephrine.

Acute Disease↗

PubMed1990

Pulsatile flow and oscillating wall shear stress in the brachial artery of normotensive and hypertensive subjects.

STUDY OBJECTIVE - The aim of the study was to examine oscillating arterial wall shear stress in hypertension. DESIGN - Pulsatile flow and oscillating wall shear stress were measured in brachial artery in hypertensive v normotensive subjects using pulsed Doppler apparatus. Methods were tested in four subjects using a micrometric procedure of Doppler probe displacement providing instantaneous real time velocity profiles. SUBJECTS - 19 ambulatory male patients with mild to moderate hypertension (diastolic blood pressure 95-114 mm Hg) and 11 normotensive male controls of similar age were studied. All were non-smokers. MEASUREMENTS and RESULTS - Arterial diameter and pulsatile centreline blood velocity were determined with pulsed Doppler, and blood viscosity was measured with a coaxial cylinder viscometer. Shear rates corresponding to maximum (gamma Vmax), minimum (gamma Vmin), and pulse (gamma Vpulse) velocities were evaluated with a simplified method of computation of Womersley equations. Corresponding shear stresses (tau Vmax, tau Vmin, tau Vpulse) were calculated as the product between shear rate and viscosity. The differences in wall shear rates obtained with the Womersley method and with the micrometric procedure were less than 10%. Compared to normotensives, hypertensives had greater arterial diameter [0.508(SEM0.006) v 0.446(0.014), p less than 0.001], lower maximum velocity [36.2(1.5) v 46.3(2.4) cm.s-1, p less than 0.001], lower absolute value of minimum velocity [-8.3(1.2) v -14.3(2.3) cm.s-1, p less than 0.01], lower pulse velocity [44.5(2.2) v 61.2(3.9) cm.s-1, p less than 0.001], and higher blood viscosity [4.77(0.08) v 4.28(0.09) mPa.s, p less than 0.001]. gamma and tau Vmax, Vmin and Vpulse were all lower in absolute value in hypertensives. Overall mean blood pressure in all subjects was negatively correlated to gamma Vmax (r = -0.65), tau Vmax (r = -0.46), gamma Vmin (r = -0.45), tau Vmin (r = -0.37), gamma Vpulse (r = -0.63), and tau Vpulse (r = -0.48). In hypertensives, age was correlated negatively to gamma Vmax (r = -0.44), tau Vmax (r = -0.46), gamma Vmin (r = -0.57), tau Vmin (r = -0.57), gamma Vpulse (r = -0.58), and tau Vpulse (r = -0.58). In normotensives, age was not correlated with shear parameters, except for tau Vmax (r = -0.60) and tau Vpulse (r = -0.66). CONCLUSIONS - The hypertensive state is associated with a reduction in oscillating wall shear in large arteries despite an increase in blood viscosity. Age in combination with hypertension also decreases wall shear conditions.

Adult↗

PubMed1990

Non-invasive evaluation of segmental pressure drop and resistance in large arteries in humans based on a Poiseuille model of intra-arterial velocity distribution.

STUDY OBJECTIVE: The aim of the study was to evaluate in hypertensive subjects the longitudinal pressure drop and segmental resistance in a large artery in relation to shearing forces of the circulating blood column at the arterial wall. DESIGN: Arterial diameter, blood velocity, and flow were measured in the brachial artery using pulsed Doppler apparatus. Blood viscosity was measured at 96 s-1 with a low shear viscometer. Segmental resistance per unit arterial length was calculated using the basic Poiseuille resistance expression from the ratio between blood viscosity and the fourth power of arterial diameter. Longitudinal pressure drop was deduced as the product between segmental resistance and blood flow. The Poiseuille model of velocity distribution also enabled wall shear rate and stress to be calculated from the ratio between blood velocity and arterial diameter and from the product between shear rate and blood viscosity respectively. PATIENTS: 19 ambulatory male patients with mild to moderate hypertension and 11 normotensive male controls of similar age were studied. RESULTS: Compared to controls, hypertensive patients had higher arterial diameter (p less than 0.001) lower blood velocity (p less than 0.05), higher blood viscosity (p less than 0.01), lower segmental resistance and pressure drop (p less than 0.001, p less than 0.01) and lower shear rate and stress (p less than 0.01, p less than 0.05). A negative correlation existed in the overall normotensive and hypertensive population between pressure drop and mean blood pressure (r = -0.55, p less than 0.01). CONCLUSION: The hypertensive state is associated with a clear reduction in large artery segmental resistance and longitudinal pressure drop concomitantly with a decrease in shear conditions at the arterial wall. The mechanisms of reduced resistance and pressure drop are related to decreased wall shear and increased diameter of the artery, both of which reduce the frictional forces at the blood-arterial wall interface.

Adult↗

PubMed1990

Abnormal wall shear conditions in the brachial artery of hypertensive patients.

Brachial artery wall shear phenomena were studied in 20 untreated essential hypertensive patients and in 11 normotensive controls of similar age. A pulsed-Doppler velocimeter was used to measure brachial artery internal diameter and mean cross-sectional and systolic centreline blood velocities. A coaxial-cylinder viscometer was used to measure blood viscosity at a shear rate of 96 s-1. A Poiseuille model of velocity distribution across the arterial lumen was used to determine wall shear rate and stress from, respectively, the ratio of blood velocity to arterial diameter and the product of shear rate and blood viscosity. Mean and systolic shear rates and stresses were calculated using, respectively, mean cross-sectional and systolic centreline blood velocities. Hypertensive patients had larger brachial artery diameters (P less than 0.001), lower systolic centreline and mean cross-sectional blood velocities (P less than 0.001, P less than 0.05), higher blood viscosity (P less than 0.001), lower mean and systolic wall shear rates (P less than 0.01, P less than 0.001) and lower systolic wall shear stress (P less than 0.05) than normotensive controls. In all subjects, mean blood pressure was negatively correlated both with mean and systolic shear rates (r = -0.38, P less than 0.05;r = -0.45, P less than 0.01). Thus the hypertensive state was associated with decreases in both mean and systolic wall shear rates, and in systolic wall shear stress. These shear abnormalities merit attention because of the atherogenic effect of low-shear conditions.

Adult↗

PubMed1990

Chronic progressive changes in brachial and carotid artery circulations under the combined effects of aging and hypertension.

Brachial and carotid artery diameters, blood velocities and blood flows were determined by a pulsed-Doppler flowmeter in 22 normotensive and 74 mild to moderate essential hypertensive subjects, aged 46 +/- 8 years. The product age x MAP/1000 (where MAP is mean arterial blood pressure), called 'arterial age' (expressed in years x mmHg/1000), was used to assess the progress of age and blood pressure. The moving-mean method was first used to explore the chronic hemodynamic changes in the two circulations with a progressive increase in arterial age. The method indicated that an arterial age of about 4-4.5 units a noticeable decrease in both brachial and carotid blood velocities occurred, and at an arterial age of about 5 units an important increase in brachial artery diameter occurred. In order to test these findings, the total sample (n = 96) was divided into three groups of equal size with low, median and high arterial ages. Brachial blood velocity decreased significantly in groups 2 (P less than 0.05) and 3 (P less than 0.05) compared with group 1, and carotid blood velocity decreased significantly from group 1 to group 2 (P less than 0.02) and from group 2 to group 3 (P less than 0.05). Brachial artery diameter did not change from group 1 to group 2, but increased significantly from group 2 to group 3 (P less than 0.05). Over the whole arterial age range, the carotid artery diameter remained identical.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

PubMed1990

Blood viscosity as a chronic contributing factor of vasodilatation in humans.

Since resistance to flow is theoretically determined by arteriolar geometry and blood viscosity, we studied these two factors in 44 normal and 106 hypertensive subjects. Brachial bed vascular resistance was calculated as the ratio between mean pressure and brachial artery flow. Systemic blood viscosity in vitro was determined at 96 per s, while microvessel blood viscosity in vivo was estimated from the haematocrit-viscosity relationship at 240 per s. A resistive radius index was calculated which was only related to the microvessel viscosity: resistance ratio. Compared to normal subjects, hypertensive subjects had higher systemic in vitro blood viscosity (4.75 +/- 0.47 versus 4.50 +/- 0.43 mPa.s; P less than 0.005) and microvessel blood viscosity (2.60 +/- 0.21 versus 2.43 +/- 0.16 mPa.s; P less than 0.001). Hypertensive subjects also had a higher brachial vascular resistance (161 +/- 89 versus 124 +/- 58 mmHg/ml per s; P less than 0.01), but showed a similar resistive radius index (2.47 +/- 0.36 versus 2.57 +/- 0.35) compared to normal subjects. There was a positive correlation between systemic viscosity and brachial artery diameter and a negative correlation between microvessel viscosity and vascular resistance in the normotensive (P less than 0.05 and P less than 0.001, respectively) and hypertensive groups (P less than 0.001 and P less than 0.005, respectively). The resistive radius index was positively related to viscosity in normal and in hypertensive groups (P less than 0.001) but these relationships were significantly different (P less than 0.001), showing that, at the highest viscosities, arterial radius increased less in hypertensive than in normal subjects. Thus, the level of blood viscosity might influence arterial diameter.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1990

[Contrary effects of hypertension and cigarette smoking on the conditions of wall shear in large arteries].

Systolic wall shear conditions were studied in the brachial artery of 4 groups of subjects including 11 non-smokers normotensives (NSNT), 25 non smokers hypertensives (NSHT), 21 smokers normotensives (SNT) and 10 smokers hypertensives (SHT). Brachial artery diameter (D) and systolic centerline blood velocity (VCLS) were measured with a pulsed Doppler device and blood viscosity at 96 sec-1 was measured with a coaxial cylinder viscometer. The wall shear rate (gamma S) corresponding to systolic velocity was calculated using a Womersley model of pulsatile flow according to the formula: alpha = (D/2) (omega/mu) 1/2, omega being the angular pulse frequency and mu the kinematic viscosity. The wall shear stress was then calculated as the product between wall shear rate and viscosity. The analysis of results in the 4 groups showed that both hypertension and smoking increased blood viscosity bu their effects on wall shear were opposite since hypertension decreased shear and stress while smoking did not change it. However, in hypertensive patients, smoking induced a clear elevation in wall shear rate and stress, whereas in smokers hypertension did not change shear conditions. Thus, opposite and interactive effects of hypertension and smokers exist on large artery wall shear phenomena which could induce differences in response of functional and structural endothelial cells to these two vascular risk factors.

Adult↗

PubMed1990

Telemetry of aortic pressure in unrestrained animals: validation of the method over a wide range of blood pressure (from 40 to 200 mmHg).

A telemetric method has been designed for continuous measurement of intra-arterial aortic blood pressure in the unrestrained dog. The system used a Konigsberg P7 transducer, a temperature-compensated voltage-controlled oscillator, an FM transmitter, and an FM tuner to convert the signal received into a voltage proportional to aortic blood pressure. The method was validated by comparison with a standard direct method (using cables for transmission). Over a wide range of blood pressure obtained by hypotensive and hypertensive drugs (in total about 2500 data points, ranging from 40 to 200 mmHg), the telemetric method gave almost the same result as the direct method. Absolute error (telemetric measure minus standard measure) was normally distributed, with a mean value of -0.44 mmHg, and a standard deviation of 3.37 mmHg. The telemetric method was designed for future studies on the chronobiology of blood pressure in normal condition, in stress conditions and under drugs.

Animals↗

PubMed1990

[A new hemodynamic endothelial approach using non-invasive evaluation of instantaneous wall shear in human arteries. Application in arterial hypertension].

A new non-invasive methodology of measurement of pulsatile wall shear in superficial large arteries in man is presented from simple determinations of internal diameter of large artery and centerline instantaneous blood velocity (pulsed Doppler apparatus) and asymptotic blood viscosity (coaxial cylinder viscometer). Pulsatile distribution of velocity across the arterial lumen has been represented by a Womersley model enabling to define and calculate wall shear rate as the slope at the wall to the velocity profile at each cardiac time. These complex mathematical calculations have been performed on micro-computer by means of appropriate programmation according to the following steps (1) Digitization and processing of instantaneous centerline blood velocity (2) Decomposition of velocity signal into Fourier series as a sum of elementary velocity sinusoids of increasing frequency (3) computation of velocity profile and slope at the wall to the profile for each harmonic (4) Resynthetization of instantaneous wall shear rate as function in time (5) calculation of wall shear stress by multiplying wall shear rate by blood viscosity. Taking the brachial artery as model of peripheral large artery, pulsatile wall shear rate and stress curves were determined in individual subjects and analysed by means of several characteristic indices including: maximum, minimum and mean values; time of systolic increase and time of systolic relaxation; and oscillating index defined from the positive and negative surfaces of the shear curve. This original methodology open new way for studying hemodynamical conditions at the interface between blood and endothelium surface of large arteries and might be applied to the physiopharmacological approach of vascular disease such as hypertension.

Adult↗

PubMed1989

Effects of nicorandil on arterial and venous vessels of the forearm in systemic hypertension.

The effects of a single oral dose of 20 mg of nicorandil were evaluated in 12 untreated patients with mild to moderate essential hypertension. Serial measurements of arterial pressures were obtained by means of an automatic device (Dynamap) up to 120 minutes after drug administration. Forearm hemodynamics were determined with a pulsed Doppler velocimeter, or strain gauge mecanography and plethysmography enabling measurement of the diameter, velocity and flow of the brachial artery as well as the arterial pulse wave velocity and forearm venous tone. In addition, local vascular resistance, compliance and impedance were deduced. Nicorandil administration produced a significant decrease in systolic and diastolic blood pressure, from 18 minutes after dosing which lasted up to the end of the study (i.e., 120 minutes after drug administration) (p less than 0.01). This decrease in blood pressure was not associated with reflex tachycardia. The brachial artery diameter increased significantly (p less than 0.01) with no change in brachial artery blood flow. A decrease in brachial-radial pulse wave velocity and arterial impedance (p less than 0.01) and an increase in arterial compliance were observed. Thus, this study demonstrated an antihypertensive activity of a single oral administration of nicorandil without baroreflex activation. This decrease in blood pressure was associated with a dilation of peripheral large arteries leading to an increase in arterial compliance. Thus, clinical testing to evaluate the antianginal activity of nicorandil, especially in hypertensive patients with coronary heart disease, should be encouraged.

Adult↗

PubMed1989

Comparative haemodynamic effects of ketanserin and ritanserin in the proximal and distal upper limb circulations of hypertensive patients.

The effects of ketanserin (40 mg p.o.) on blood pressure and brachial haemodynamics (brachial artery diameter, brachial blood velocity and blood flow) have been compared in a double-blind study with those of ritanserin (10 mg p.o.) and placebo. Haemodynamic parameters were measured before and 1 h after treatment. Patients with mild to moderate essential hypertension participated in this study, 6 each on ketanserin, ritanserin and placebo. Placebo significantly reduced heart rate and did not modify the other parameters. Compared to placebo, ketanserin significantly reduced systolic and diastolic blood pressure, increased brachial blood velocity and flow, and decreased forearm vascular resistance. Compared to placebo, ritanserin slightly decreased blood pressure and slightly increased blood flow, but neither effect was significant. When blood circulation to the hand was excluded, neither ketanserin nor ritanserin modified the proximal arterial resistance or blood flow. It is concluded that the actions of ketanserin and ritanserin essentially occurred in the distal part of the upper limb, and alpha 1-receptor blockade is probably involved.

Arm↗

PubMed1989

Preload, adrenergic activity, and aortic compliance in normal and hypertensive patients.

Aortic compliance is a major determinant of systolic blood pressure and of impedance to left ventricular ejection. However, little is known about its regulating factors. To assess the effects of preload and adrenergic activity on aortic compliance, we studied 10 normal subjects and nine untreated hypertensive patients at rest and during lower body negative pressure. Aortic compliance was measured invasively from the diastolic decay of the aortic pressure tracing and systemic vascular resistance. Preload was decreased stepwise by lower body negative pressure (-5 to -40 mm Hg) while adrenergic activity was assessed by the change in plasma norepinephrine at a maximum level of negative pressure suction. At rest, aortic compliance was lower in hypertensive subjects compared with its value in normal individuals (0.048 +/- 0.012 [SD] versus 0.071 +/- 0.009 units, p less than 0.001) but correlated inversely with systolic blood pressure in both groups (r = -0.64 in normotensive individuals, r = -0.83 in hypertensive subjects, r = -0.88 for the whole group, p less than 0.001 for all). Whereas resting pulmonary wedge pressure was higher in hypertensive subjects compared with normal individuals (16 +/- 4 [SD] versus 11 +/- 3 mm Hg, p less than 0.05), resting plasma norepinephrine levels were not different between the two groups (261 +/- 139 versus 251 +/- 103 pg/ml). Neither of these two resting indices correlated with baseline aortic compliance in both normotensive individuals and hypertensive patients. During lower body negative pressure (LBNP), cardiac filling pressure (right atrial pressure and pulmonary wedge pressure) as well as cardiac output decreased in the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Aorta↗

PubMed1989

Comparative long-term vasoactive effects of atenolol and carteolol on the properties of the small and large arteries of the upper extremities in human essential hypertension.

The long-term effects of selective (atenolol) and nonselective (carteolol) beta-blockers on brachial artery diameter velocity and flow and on vascular resistance (pulsed Doppler) were compared in two groups of 10 hypertensive patients at respective daily doses of 100 and 20 mg. The drugs decreased mean blood pressure (p less than 0.01) with similar magnitude, although systolic blood pressure was decreased more by atenolol than by carteolol (p less than 0.05). Heart rate was decreased by atenolol (p less than 0.01) but was unchanged by carteolol. The drugs did not change brachial circulation when the hand circulation was present. During hand exclusion (wrist occlusion) comparison from baseline showed that atenolol decreased velocity and flow (p less than 0.01, p less than 0.05) and increased resistance (p less than 0.05), whereas carteolol decreased resistance (p less than 0.05); after 3 months of treatment, velocity and flow were higher (p less than 0.01, p less than 0.001) and resistance was lower (p less than 0.01) with carteolol than with atenolol. Thus, hand exclusion demonstrated opposite drug effects on arterioles--dilation for carteolol and constriction for atenolol.

Adult↗

PubMed1989

Platelet cytosolic proton and free calcium concentrations in essential hypertension.

Alterations in the metabolism of intracellular messengers, such as calcium and cyclic adenosine 5'-phosphate (cAMP), have been reported in essential hypertension. Since intracellular pH (pHi) participates in the control of fundamental cell functions, we looked for changes in platelet cytosolic H+ concentration [( H+]i) in hypertension and investigated whether or not its impaired metabolism is linked to the calcium handling abnormalities. The fluorescent pH indicator BCECF has been used to evaluate intracellular H+ concentration in platelets, unstimulated ex vivo, from normotensive (n = 20) and hypertensive patients (n = 20). Cytosolic [H+] was 20% lower in hypertensive than in normotensive subjects (49.5 +/- 3.4 and 61.8 +/- 2.2 nmol/l cells, respectively, P less than 0.005; mean pHi values were 7.21 and 7.33, respectively). Platelet cytosolic H+ and free Ca2+ concentrations ([Ca2+]i) were determined in parallel in 15 normotensive and 15 hypertensive patients. [Ca2+]i was found to be 19% higher (P less than 0.01), and [H+]i 22% lower (P less than 0.02), in the hypertensive patients compared with the normotensive subjects. Platelet pHi and [Ca2+]i were increased simultaneously in some hypertensive patients. These results are compatible with the hypothesis of an in vivo activation of platelets in hypertension. If a similar alkalinization exists in smooth muscle cells, it may participate in cell proliferation and in an enhanced sensitivity to agonists, two parameters thought to be involved in blood pressure elevation.

Adult↗