Showing papers by "Athanase Benetos published in 1993"
TL;DR: Noninvasive in situ evaluations of pulsatile changes of blood pressure and arterial diameter were performed at the sites of the common carotid and femoral arteries in a population of 78 untreated normotensive and hypertensive subjects.
Abstract: Noninvasive in situ evaluations of pulsatile changes of blood pressure and arterial diameter were performed at the sites of the common carotid and femoral arteries in a population of 78 untreated normotensive and hypertensive subjects. Arterial segments were studied by using an original echo-tracking technique for internal diameter and validated applanation tonometry for local pulse pressure measurements. Whereas mean arterial pressure is known to be identical in all parts of the arterial tree, pulse pressure was significantly lower in the carotid (52.7 +/- 2.2 mm Hg) than in the brachial (62.0 +/- 2.0 mm Hg) or femoral (62.5 +/- 2.5 mm Hg) arteries. Despite a higher pulse pressure and diastolic diameter, the femoral artery had a lower pulsatile change in diameter (3.47 +/- 0.18% versus 6.07 +/- 0.28%; p < 0.0001) and distensibility coefficient (9.36 +/- 0.58 versus 21.60 +/- 1.75 x 10(-3) kPa-1) than the carotid artery. Local cross-sectional compliance of the carotid artery was higher than that of the femoral artery (7.42 +/- 0.46 versus 6.20 +/- 0.28 m2.kPa-1.10(-7); p < 0.05). Whereas age was strongly correlated with arterial parameters at the site of the carotid artery (pulse pressure: r = 0.54, p < 0.0001; pulsatile change in arterial diameter: r = -0.62, p < 0.0001; distensibility coefficient: r = -0.70, p < 0.0001), no significant correlation was observed at the femoral artery. Mean blood pressure was the second factor of carotid artery alterations: the higher the mean blood pressure, the lower the distensibility of this artery (r = -0.36, p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
607 citations
TL;DR: Evidence was found that although felodipine had specific effects on the arterial system of hypertensive subjects, hydrochlorothiazide did not produce any sizable arterial change, and differential effects may influence specifically the heart afterload.
Abstract: In a double-blind cross-over study, the arterial changes produced by hydrochlorothiazide were compared with those observed after the calcium antagonist felodipine in 16 patients with mild to moderate systemic hypertension Diameter changes at the site of the common carotid and brachial arteries were investigated using pulsed Doppler velocimetry, and pulse-wave velocities of the aortic, brachial and femorotibial areas were measured using standard noninvasive techniques Whereas hydrochlorothiazide and felodipine similarly decreased blood pressure, hydrochlorothiazide did not change pulse-wave velocity, and the diameters of the brachial and common carotid arteries Felodipine significantly decreased pulse-wave velocity, and increased brachial arterial diameter and compliance, with no change in carotid arterial diameter Evidence was found that although felodipine had specific effects on the arterial system of hypertensive subjects, hydrochlorothiazide did not produce any sizable arterial change These differential effects may influence specifically the heart afterload, with important consequences for diuretics that are known to cause minimal changes in cardiac structure and function
70 citations
TL;DR: With aging there is an increased vasoconstricting effect of alpha-agonists and a decreased vasodilatative action ofalpha-blockade, which is suggested to be linked to the regulation of carotid arterial compliance.
Abstract: The present study was designed to assess the role of the adrenergic tone in the regulation of carotid arterial compliance during aging. An experimental model of in situ isolated carotid arteries has been used to evaluate the elastic properties of the arterial wall in young (3-mo-old) and older (18-mo-old) Wistar rats. Binding experiments were performed in the same strain of rats to evaluate alpha 1- and beta-adrenoceptor affinity and density. In a third set of experiments, structural parameter of the carotid artery in younger and older rats was evaluated. Arterial distensibility (compliance per unit of volume) was significantly lower in older rats. This was associated with a significant thickness of the media (45.6 +/- 2.8 vs. 57.5 +/- 5.7 microns, P < 0.01) and increased collagen content in older rats (4,420 +/- 310 vs. 7,320 +/- 850 microns 2/mm, P < 0.001). However, carotid arterial compliance was not altered in older rats because of the significant increase in cross-sectional area with aging. Aging did not affect alpha 1-adrenoceptor affinity and density, whereas it decreased beta-density without changing their affinity. Pharmacological stimulation of alpha 1-adrenoceptor with phenylephrine (10(-5) M) decreased compliance in older but not in younger animals. Blockade of these receptors with prazosin or labetalol increased compliance in younger and had no effect on older rats. beta-receptor stimulation with isoproterenol or blockade with propranolol had no effect in any of the studied groups. We suggest that with aging there is an increased vasoconstricting effect of alpha-agonists and a decreased vasodilatative action of alpha-blockade.(ABSTRACT TRUNCATED AT 250 WORDS)
34 citations
TL;DR: A previously described model of the in situ carotid artery was used to determine the pressure-volume relationship over a range of transmural pressures in normotensive rats (WKY) and spontaneously hypertensive Rats (SHR) and the total relaxation of arterial smooth muscle was achieved after a local administration of potassium cyanide.
Abstract: Acute converting enzyme inhibition relaxes arterial smooth muscle and increases arterial complicance in several models of animal and human hypertension. However, it is unknown whether the doses needed
19 citations
TL;DR: The results suggest that the measurement of pulse pressure may be an available index to differentiate normotensive and hypertensive rats, and that increased aortic pulse pressure in SHR participates in the increase in cardiac afterload independently of mean arterial pressure, and may be a preferential site of action of antihypertensive agents.
Abstract: BACKGROUND In large animals pulse pressure increases from central to peripheral arteries whereas mean arterial pressure decreases slightly. This haemodynamic pattern has not been verified in small animals, particularly in hypertensive rats before and after administration of antihypertensive drugs. DESIGN The intra-arterial blood pressure of normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) was determined along the aorta in anaesthetized and conscious rats. In anaesthetized rats the study was performed before and after acute intravenous nicardipine administration (30 micrograms/kg). RESULTS Mean arterial pressure was significantly higher in untreated SHR than in WKY rats, and within each strain was quite similar along the aortic tree. Pulse pressure increased significantly from the central to the terminal aorta in WKY rats, principally due to an increase in systolic blood pressure. In SHR pulse pressure did not differ along the aortic tree. Compared with in WKY rats, aortic pulse pressure in SHR was significantly elevated whereas femoral pulse pressure was quite similar. Acute nicardipine administration re-established the pulse pressure gradient in SHR, due to a significant decrease in central aortic pulse pressure with no significant change in femoral pulse pressure. CONCLUSIONS These results suggest, first, that since there are large differences in pulse pressure in the proximal aorta of SHR and WKY rats but only small or negligible differences in the distal aorta, the measurement of pulse pressure may be an available index to differentiate normotensive and hypertensive rats, and secondly, that increased aortic pulse pressure in SHR participates in the increase in cardiac afterload independently of mean arterial pressure, and may be a preferential site of action of antihypertensive agents.
13 citations
TL;DR: The findings confirm the higher meteorological dependence of hemodynamics in the elderly, and suggest that the research protocols using the cold pressor test should adjust the response for the previous environmental temperature.
11 citations
TL;DR: Results show that endogenous BK has a vasodepressor effect on DS rats fed a low NaCl diet and this effect is suppressed after a high-salt diet, which is suggested to be implicated in NaCl-induced hypertension in salt-sensitive animals.
Abstract: We assessed the participation of endogenous bradykinin (BK) on basal blood pressure (BP) regulation in anesthetized Dahl-sensitive (DS) and Dahl-resistant (DR) rats receiving different NaCl diets. Four groups of Dahl rats were studied after 5 weeks of high (H) = 7% or low (L) = 0.4% NaCl diet (DSH, n = 9; DSL, n = 11; DRH, n = 9; DRL, n = 10). Endogenous BK activity was assessed with a continuous intraarterial (i.a.) infusion of the specific BK antagonist (B4146 100 micrograms/kg/min) for 10 min. Sensitivity to exogenous BK was tested 30 min after the end of the infusions, with bolus intraarterial (i.a.) injections of BK (0.1, 0.5, 1, and 5 micrograms). DSH had a significantly higher (p < 0.0001) basal mean BP (MBP) as compared with the three other groups: DSH = 185 +/- 7 mm Hg (mean +/- SEM), DSL = 143 +/- 5 mm Hg, DRH = 132 +/- 10 mm Hg, and DRL = 134 +/- 6 mm Hg. BK antagonist infusion increased MBP by 13.2 +/- 1.5 mm Hg in DSL rats, by 6.8 +/- 1.6 mm Hg in DRL, by 4.7 +/- 1.6 mm Hg in DRH, and by 1.1 +/- 8 mm Hg in DSH. Statistical analysis showed that the high NaCl diet significantly decreased the response to the BK antagonist in DS (p < 0.001) but not in DR rats. MBP response to exogenous BK was similar in all groups. These results show that endogenous BK has a vasodepressor effect on DS rats fed a low NaCl diet. This effect is suppressed after a high-salt diet.(ABSTRACT TRUNCATED AT 250 WORDS)
4 citations
TL;DR: It appears that approximately one out of four normotensive subjects and one-half of all hypertensive patients are sensitive to salt, with their blood pressure increasing following excessive salt intake.
Abstract: The concept that a high salt intake is related to increased prevalence of hypertension is an old one. There is enough epidemiological, clinical, historical and experimental evidence to support this concept [1–3]. Most authorities currently believe that excessive salt intake is the first environmental risk factor for hypertension [4]. It appears that approximately one out of four normotensive subjects and one-half of all hypertensive patients are sensitive to salt, with their blood pressure increasing following excessive salt intake [5–7].
1 citations