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The objective of this feasibility study is to evaluate the use of the 'Physilog' device, an ambulatory physical-activity recorder based on acceleration measurement, for the monitoring of daily physical activities. Accelerations measured at the level of the chest and the thigh are recorded by Physilog over a period of 1 h in five normal subjects. A specially designed studio-like room allowing the performance of most usual activities of everyday life is used. A video film synchronised with the Physilog is obtained for each subject to check the accuracy of the data derived from Physilog. Based on the analysis on the average and the deviation of the acceleration signal, an algorithm is developed to classify the activities in four categories, i.e. lying, sitting, standing and locomotion. Compared with the video observations, the results from the algorithm show an overall misclassification of 10.7%, which is mainly due to confusion between dynamic activities and the standing posture. In contrast, the misclassification between postures is negligible. It is concluded that Physilog can be used in the clinical setting for the reliable measurement and long-term recording of most usual physical activities.

The goal of this study was to investigate whether the elastic behavior of conduit arteries of humans or rats is altered as a result of concomitant hypertension. Forearm arterial cross-sectional compliance-pressure curves were determined noninvasively by means of a high precision ultrasonic echo-tracking device coupled to a photoplethysmograph (Finapres system) allowing simultaneous arterial diameter and finger blood pressure monitoring. Seventeen newly diagnosed hypertensive patients with a humeral blood pressure of 163/103 +/- 4.4/2.2 mm Hg (mean +/- SEM) and 17 age- and sex-matched normotensive controls with a humeral blood pressure of 121/77 +/- 3.2/1.9 mm Hg were included in the study. Compliance-pressure curves were also established at the carotid artery of 16-week-old anesthetized spontaneously hypertensive rats (n = 14) as well as Wistar-Kyoto normotensive animals (n = 15) using the same echo-tracking device. In these animals, intra-arterial pressure was monitored in the contralateral carotid artery. Mean blood pressures averaged 197 +/- 4 and 140 +/- 3 mm Hg in the hypertensive and normotensive rats, respectively. Despite the considerable differences in blood pressure, the diameter-pressure and cross-sectional compliance-pressure and distensibility-pressure curves were not different when hypertensive patients or animals were compared with their respective controls. These results suggest that the elastic behavior of a medium size muscular artery (radial) in humans and of an elastic artery (carotid) in rats is not necessarily altered by an increase in blood pressure.

This study was designed to evaluate in healthy volunteers the renal hemodynamic and tubular effects of the orally active angiotensin II receptor antagonist losartan (DuP 753 or MK 954). Losartan or a placebo was administered to 23 subjects maintained on a high-sodium (200 mmol/d) or a low-sodium (50 mmol/d) diet in a randomized, double-blind, crossover study. The two 6-day diet periods were separated by a 5-day washout period. On day 6, the subjects were water loaded, and blood pressure, renal hemodynamics, and urinary electrolyte excretion were measured for 6 hours after a single 100-mg oral dose of losartan (n=16) or placebo (n=7). Losartan induced no significant changes in blood pressure, glomerular filtration rate, or renal blood flow in these water-loaded subjects, whatever the sodium diet. In subjects on a low-salt diet, losartan markedly increased urinary sodium excretion from 115±9 to 207±21 ^unol/min (P<.05). The fractional excretion of endogenous lithium was unchanged, suggesting no effect of losartan on the early proximal tubule in our experimental conditions. Losartan also increased urine flow rate (from 10.5 ±0.4 to 13.1±0.6 mL/min, P<.05); urinary potassium excretion (from 117±6.9 to 155±11 /tmol/min); and the excretion of chloride, magnesium, calcium, and phosphate. In subjects on a high-salt diet, similar effects of losartan were observed, but the changes induced by the angiotensin II antagonist did not reach statistical significance. In addition, losartan demonstrated significant uricosuric properties with both sodium diets. Urinary uric acid excretion increased from 3.5±0.2 to 11.1 ±0.5 /imol/min (P<.01) in salt-depleted subjects and from 3.1 ±0.2 to 9.66±0.6 /tmol/min (/ > <.01) in salt-loaded volunteers. This marked uricosuric effect of losartan was associated with a decrease in plasma uric acid. The time course of these changes in uric acid excretion suggests that it is a property of the parent compound rather than of a metabolite. These results demonstrate that in healthy subjects the angiotensin II receptor antagonist losartan is a natriuretic and kaliuretic compound, in particular during salt depletion. Moreover, losartan promotes uric acid excretion, an effect that appears to be independent of angiotensin II blockade.

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