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Biomedical subjects

S Laurent

Publications and source records attributed to S Laurent.

At least 217 records · Page 12Linked to original sources
PubMed1988

Increased response of brachial artery diameter to norepinephrine in hypertensive patients.

The hyperresponsiveness of small arteries to norepinephrine is well documented in essential hypertensive patients. Our objective was to investigate in situ the reactivity to norepinephrine of the diameter of large arteries, which are involved in the arterial disease of hypertension as well as small arteries. Brachial artery diameter, blood flow velocity, local volumic blood flow, and local vascular resistances were determined noninvasively with a pulsed Doppler system in 19 patients with essential hypertension and 9 normotensive subjects, before and after the administration of placebo (glucose) or increasing doses of norepinephrine (10, 20, and 40 ng.kg-1.min-1 iv) given in a single-blind fashion. In hypertensive patients, norepinephrine (40 ng.kg-1.min-1) induced 1) a significant decrease in brachial artery diameter, local blood velocity, volumic flow, and conductance and 2) a small increase in mean arterial pressure. These hemodynamic changes did not occur in the placebo group and were significantly greater in hypertensive patients than in normotensive subjects, although plasma norepinephrine increased to the same extent in both groups. We conclude that in hypertensive patients the increase in vascular reactivity to norepinephrine involves not only the resistive vessels but also the large arteries thus decreasing their conducting and buffering function.

Adult↗
PubMed1988

Reversion of cardiac hypertrophy and reduced arterial compliance after converting enzyme inhibition in essential hypertension.

Blood pressure, forearm arterial hemodynamics (with a pulsed Doppler flowmeter), and echocardiographic parameters were studied in 16 patients with sustained essential hypertension before and 3 months after administration of the converting enzyme inhibitor perindopril. In a single-blind study versus placebo, it was shown that perindopril significantly reduced blood pressure (p less than 0.01), whereas there was an increase in brachial blood flow (p less than 0.01) because of a simultaneous increase in blood flow velocity (p less than 0.01) and arterial diameter (p less than 0.01). During a 5-minute period of wrist occlusion, blood flow velocity was reduced to a greater extent with perindopril than with placebo (p less than 0.001), whereas corresponding reductions in arterial diameter were equivalent, indicating that the increase in diameter after perindopril could not be explained simply on the basis of flow-dependent dilatation. During active treatment, brachial artery compliance increased (p less than 0.01) and pulse wave velocity decreased (p less than 0.01), whereas there was no change in the tangential tension of the arterial wall, defined as the product of mean arterial pressure and arterial diameter. Four weeks after treatment was stopped, blood pressure and forearm arterial hemodynamics returned toward baseline values. Cardiac mass was significantly decreased after perindopril (p less than 0.01) and remained decreased 4 weeks after cessation of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Hemodynamics of the carotid artery after vasodilation in essential hypertension.

We performed simultaneous noninvasive measurements of common carotid artery and brachial artery hemodynamics in nine normal subjects and 10 subjects with sustained essential hypertension. In hypertensive subjects, brachial artery blood flow and forearm vascular resistance were in the normal range while carotid artery blood flow and carotid artery resistance were decreased and increased, respectively. The most important findings were the changes in the internal caliber of large arteries. Although the brachial and carotid artery diameters of hypertensive subjects were measured for the same level of mean arterial pressure, brachial artery diameter was significantly increased and carotid artery diameter was strictly normal as compared with values found in normal subjects. To assess whether carotid artery circulation could influence the baroreceptor reflex response to arteriolar vasodilation, carotid artery and brachial artery hemodynamics were measured in immediate succession in normotensive and hypertensive subjects before and after oral administration of cadralazine, a dihydralazine derivative. After cadralazine treatment, carotid artery tangential tension decreased in hypertensive subjects, and the changes were significantly correlated to the increase in heart rate. A similar correlation was found in normal subjects, but it was reset toward higher heart rates. These results indicate that the carotid artery does not behave like the brachial artery in response to a chronic increase in blood pressure. This behavior indicates intrinsic alterations of the arterial wall and might be involved in the resetting of the carotid baroreceptor reflex. Carotid artery circulation could play a role in hypertension by modulating the carotid baroreceptor mechanisms involved in the response to drug-induced arteriolar vasodilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Central modulation of baroreceptor reflex response to phenylephrine by dihydropyridines in rats.

The effects of two dihydropyridine derivatives, the calcium channel agonist BAY k 8644 or the antagonist PN 200-110, on the central nervous components of the baroreceptor reflex control of heart rate during activation of baroreceptors by phenylephrine (2 micrograms i.v.) were studied in pentobarbital-anesthetized normotensive (Wistar) rats and spontaneously hypertensive rats (SHR). To rule out an effect on peripheral vessels or on the sinoauricular node (or on both), BAY k 8644 and PN 200-110 were administered intracerebroventricularly (i.c.v.) at doses that did not change blood pressure. Baroreceptor reflex sensitivity was calculated as the slope of the relationship between systolic arterial pressure and heart period. Baroreceptor reflex sensitivity increased with time following the onset of anesthesia. In SHR, injection of BAY k 8644 (3 micrograms/kg i.c.v.) suppressed the time-dependent increase in baroreceptor reflex sensitivity. The inhibitory effect of BAY k 8644 (3 micrograms/kg i.c.v.) on the time-dependent increase in baroreceptor reflex sensitivity was suppressed by pretreatment with PN 200-110 (0.6 microgram/kg i.c.v.) but not with the solvent, indicating that the central effect of BAY k 8644 occurred at the level of specific dihydropyridine binding sites. In addition, the inhibitory effect of BAY k 8644 (3 micrograms/kg i.c.v.) on the time-dependent increase in baroreceptor reflex sensitivity was suppressed by pretreatment with the muscarinic antagonist atropine methylnitrate (80 micrograms/kg i.c.v.) but not with the solvent. In normotensive rats, the time-dependent increase in baroreceptor reflex sensitivity was not significantly altered by BAY k 8644 (3 micrograms/kg i.c.v.).(ABSTRACT TRUNCATED AT 250 WORDS)

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1988

[Central control of the baroreflex response to phenylephrine by dihydropyridines in the anesthetized rat].

We have previously shown that a calcium channel activator (BAY K 8644) and a calcium channel inhibitor (CCI) (nifedipine), both dihydropyridine derivatives (DHP), can modulate in opposite fashion calcium dependent mechanisms involved in the central control of blood pressure and heart rate in SHR but not in Wistar rats. These results suggested that central DHP receptor sites might modulate baroreflex function. Therefore, we studied in pentobarbital anaesthetized SHR, the effects of BAY K 8644 and PN (200-110) (CCI) on central integration of baroreflex function (ramp method: phenylephrine 2 microgram i.v.). In order to rule out peripheral vascular effects, BAY and PN were administered intracerebroventricularly (i.c.v.) at doses which did not change BP. Baroreflex sensitivity (BRS) increased with time following the onset of anesthesia. In SHR, i.c.v. injection of BAY (3 microgram/kg) but not PN (0.6 micrograms/kg) suppressed the time dependent increase in BRS. The inhibitory effect of BAY on the time-dependent increase in BRS was suppressed by a pretreatment with PN (0.6 micrograms/kg i.c.v.) and by a pretreatment with the muscarinic antagonist atropine methylnitrate (80 micrograms/kg i.c.v.). BAY i.c.v. dit not change BRS in Wistar rats. These results indicate that DHP may centrally modulate BRS in SHR and suggest a central sympatho-excitatory effect for BAY mediated by an enhanced release of acetylcholine.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1988

[Atrial natriuretic factor diminishes the contractility of the cardiac cell in culture].

The hypotensive effect of ANP has been associated with lowered cardiac output. Although only minor or no negative inotropic effect was found in vitro, a direct myocardial depressant effect of ANP remains a possible mechanism in vitro, in addition to the reduction in cardiac preload. Therefore we tested the hypothesis of a direct negative inotropic effect of ANP on the cultured chick embryo ventricular cell, an experimental system which contains no neural elements and no endogenous neurotransmitters. ANP (rat-ANP 1-23) 10(-8) M significantly and reversibly decreased contractility in spontaneously beating cells. A further decrease (-30 +/- 4 p. 100 of initial amplitude of contraction) was observed at 2.5 x 10(-7) M: -17 +/- 4 p. 100 of initial amplitude). The positive inotropic effect of angiotensin II (2.5 x 10(-7) M) on spontaneously beating cells was fully antagonized by ANP (2.5 x 10(-7) M) and amplitude of contraction decreased under control levels. By contrast (1) the increase in contractility in response to extra-cellular calcium (increased from 1.5 to 2.1 mM) was significantly less altered by ANP and (2) the time-course of the positive inotropic effect of the calcium-channel agonist BAY K 8644 (5 x 10(-9) M) or the beta-adrenergic agonist isoproterenol (10(-6) M) was unchanged by ANP. These results indicate a direct negative inotropic effect of ANP (1-23) on cultured chick heart cells and suggest an effect on intracellular messengers involved in the cardiac effects of angiotensin II.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1988

[Effects of beta-blockers on hemodynamics of the forearm after tobacco stimulation].

In mild hypertension, a betablocker treatment could reduce cardiovascular events. But in smoking men the benefit disappears and this interaction is unexplained. In 6 healthy non smoking men, we studied the effects of acute oral administration of propranolol (80 mg) pindolol (15 mg) and placebo after cigarette smoking (CS) (two cigarettes within 10 minutes). In a double blind cross over randomized study, arterial pressure and heart rate (HR) were recorded within 20 minutes after CS. Brachial artery diameter (D), Local vascular Resistance (RL), Local arterial Compliance (CL) and pulse wave velocity (VOP) were determined non invasively (using a pulsed doppler system) before and 20 mn after CS. Under placebo, mean arterial pressure (PAM), HR and RL increased significantly after CS (+9.2 +/- 3 mmHg, +4.5 +/- 3 b/mn and +36 +/- 14 per cent, respectively). These modifications were not different after propranolol, pindolol or placebo (ANOVA). Arterial distensibility (CL) was decreased after CS and this alteration was not prevented by beta-blockers. Brachial artery diameter was not modified after CS. Our results demonstrate that acute treatment with non selective beta-blockers with or without sympathomimetic intrinsic activity does not prevent haemodynamic modifications induced by cigarette smoking.

Adrenergic beta-Antagonists↗
PubMed1988

[Pulse wave velocity and ambulatory blood pressure in essential arterial hypertension].

Cardiovascular morbidity and mortality of hypertensive patients is mainly related to lesions of large arteries. Arterial distensibility estimated by carotid-femoral pulse wave velocity (PWV) was evaluated in 22 patients with sustained essential hypertension, together with three different methods of blood pressure (BP) measurement: mercury sphygmomanometer, semi-automatic BP recording using the Dinamap apparatus and 24 H ambulatory BP monitoring using the Spacelabs Monitor (5200). Table shows that, while PWV was not correlated with BP measured by mercury sphygmomanometer, it was strongly and positively correlated with BP measured by the other procedures. The best correlation coefficient was noted for the systolic BP measured in the Day Time (7 h-22 h) by the ambulatory method. This study shows that BP Monitoring correlates more strongly than clinic or casual BP with indices of target organ damage. (Table: see text).

Adult↗
PubMed1988

[Pulse pressure and echocardiographic parameters in essential arterial hypertension].

UNLABELLED: We measured systolic, diastolic, mean (MAP) and pulsed (PP) arterial pressures (Dinamap 845 XT), carotid femoral pulse wave velocity (PWV) and cardiac parameters (echocardiography) to evaluate myocardiac mass and indexed cardiac mass to body surface area (IM) in 47 subjects (11 normotensives and 36 with sustained essential hypertension). Hypertensives were allocated between two groups with same age, weight and height, same mean arterial pressure (119.8 +/- 9.1 mmHg, 119.7 +/- 11.9 mmHg, NS) and PWV (11.90 +/- 2.20 m/s, 12.51 +/- 1.83 m/s, NS): group I (22 subjects) with pulsed pressure less than 60 mmHg, group II (14 subjects) with pulsed pressure greater than or equal to 60 mmHg. (Table: see text). Newman-Keuls between group I and group II: p less than 0.01 for cardiac mass and IM, p less than 0.001 for PP. Cardiac mass (p less than 0.01) and indexed mass to body surface area (p less than 0.01) were greater in group II (with pp greater than or equal to 60 mmHg) than in group I. CONCLUSION: arterial hypertension is linked with left ventricular hypertrophy which is increased when pulsed pressure is enhanced. This fact could give evidence of importance of pulsatory work in cardiac consequence of hypertension.

Adult↗
PubMed1988

[Flow-dependent vasodilation of the brachial artery in the normotensive and essential hypertensive patient].

Brachial artery hemodynamics including brachial artery diameter (D), local blood flow velocity (V) and local volumic blood flow, was studied in 10 normotensive subjects (NT) and 10 age-matched hypertensive patients (HT) (50 +/- 4 vs 43 +/- 4 years; m +/- SEM; NS), using a bidimensional pulsed doppler system at rest (control period), during a 2 (or 4) mn-period of distal circulatory occlusion (DO) and during the following reactive hyperemia (RH). Kinetics of change in blood flow velocity and diameter were determined during successive and reproducible manoeuvres. V and D decreased significantly during DO. During RH (1) V reached similar maximum values in both groups (after 2 mn DO: NT: from 2.4 +/- 1.1 to 19.0 +/- 6.9 cm/s; HT: from 2.9 +/- 0.8 to 17.2 +/- 7.6 cm/s) and (2) D increased significantly in both groups (after 2 mn DO: NT: from 0.395 +/- 0.016 to 0.450 +/- 0.025 cm; p less than 0.001; HT: from 0.408 +/- 0.018 to 0.467 +/- 0.018 cm; p less than 0.001), reaching levels significantly higher than during the control period. The brachial artery vasodilation observed in both groups (NT: +12 +/- 3 p. 100; HT: +15 +/- 3 p. 100 of initial diameter) was significantly greater (p less than 0.001), than the reproducibility of the diameter measurement (3 +/- 1 p. 100). Mean arterial pressure and heart rate dit not change during the whole investigation. Increasing the duration of DO from 2 to 4 mn further enhanced the reactive blood flow velocity but did not change the magnitude of the reactive brachial artery vasodilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Central interactions between dihydropyridines and cholinergic systems in the control of blood pressure in rat.

Intracerebroventricular (i.c.v.) injection of the 1,4-dihydropyridine (DHP) calcium channel agonist, Bay K8644 (30 micrograms/kg) increased mean blood pressure and the K+-evoked release of [3H]acetylcholine ([3H]ACh) from hippocampal slices in spontaneously hypertensive rats (SHR). The Bay K8644-induced hypertension was inhibited by a pretreatment with methylatropine (80 micrograms/kg i.c.v.). In SHR, nicardipine, a DHP calcium channel antagonist, reduced mean blood pressure when i.c.v. injected (10 micrograms/kg). The nicardipine-induced hypotension was reduced by a pretreatment with hemicholinium-3 (20 micrograms, i.c.v.). Nicardipine (1 microM) did not modify, in SHR, the K+-evoked release of [3H]ACh, but inhibited the Bay K8644-induced increase in the ACh release. In normotensive rats, neither Bay K8644 nor nicardipine modify blood pressure, when centrally injected, or the stimulated release of [3H]ACh from hippocampal slices. The participation of central DHP sites in the cholinergic transmission in genetic hypertension is discussed.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1987

[Current treatment regimen in essential arterial hypertension].

The introduction in the treatment of arterial hypertension of angiotensin-converting enzyme inhibitors and calcium inhibitors, as well as the results of extensive multicentric therapeutic trials, suggest that the prescription of antihypertensive drugs will be profoundly altered in the forthcoming years. The "step by step" approach will be abandoned, and each patient will receive one or two drugs chosen for being the most selective and most suitable for his case. These more personalized long-term treatments will be better tolerated, and the greater patient's compliance will make them more effective drugs to the underlying pathology (smoking habits, blood lipid disorders, early arterial lesions) the antihypertensive treatment will have a greater reducing effect on cardiovascular morbidity and mortality.

Antihypertensive Agents↗
PubMed1987

Brachial artery cross-sectional area and distensibility before and after arteriolar vasodilatation in men with sustained essential hypertension.

Blood pressure, volume distensibility (VD), and cross-sectional area (CSA) of the brachial artery were studied using pulsed Doppler systems in 51 patients with sustained essential hypertension in comparison with 21 normotensive controls of the same age. In hypertensive patients, in baseline conditions, CSA was significantly increased and VD decreased--the two parameters strongly and negatively correlated independent of the blood pressure level. Arteriolar vasodilatation was produced by three pharmacological agents--cadralazine, a dihydralazine-like compound; nicorandil, a nicotinamide derivative; and nitrendipine, a calcium entry blocker. For the same blood pressure reduction, cadralazine significantly reduced CSA, while nicorandil and nitrendipine increased it. Nitrendipine significantly increased VD, which was not modified by cadralazine and nicorandil. For cadralazine and nicorandil, a significant negative correlation was observed between VD and CSA. The relationship was the same as in baseline conditions. With nitrendipine, no significant correlation was observed between the two parameters. At any given CSA, distensibility was higher with nitrendipine than with cadralazine or nicorandil. The study provided evidence that, in men with essential hypertension, in basal conditions, the negative relationship between VD and CSA reflected intrinsic alterations of the arterial wall, while cadralazine, nicorandil, and nitrendipine caused a similar degree of arteriolar dilatation, nicorandil and nitrendipine caused active arterial dilatation as well, and changes in distensibility after drug administration were not directly related to blood pressure level and were mediated either by predominant geometrical modifications (cadralazine, nicorandil) or by the predominant relaxing effect of the drug on arterial smooth muscle tone (nitrendipine), or both.

Adult↗
PubMed1987

Captopril + hydrochlorothiazide 24 h ambulatory monitoring effects.

The purpose of this study was to evaluate over a 24 h period the antihypertensive effect of captopril 50 mg + hydrochlorothiazide (HCTZ) 25 mg once a day in mild to moderate hypertension. Ambulatory recordings over 24 h of the blood pressure using the Spacelabs system were performed, at the end of a 15-day placebo period and after giving captopril + HCTZ for 45 days. Captopril + HCTZ significantly decreased (P less than 0.001) systolic and diastolic blood pressures for both the diurnal period (8 h to 22 h) and the nocturnal period (22 h to 8 h). No change in heart rate was observed. For further analysis, the mean hour values of blood pressure and heart rate were calculated. A constant decrease of the systolic and diastolic blood pressure throughout the 24 h was obtained after captopril + HCTZ without any change in heart rate and in nyctohemeral variations. The study provided evidence that, in patients with mild to moderate essential hypertension, captopril + HCTZ once a day decreased systolic and diastolic blood pressure all day long without any change in the heart rate and the blood pressure nyctohemeral cycle.

Adult↗
PubMed1987

Opposite central cardiovascular effects of nifedipine and BAY k 8644 in anesthetized rats.

The central cardiovascular effects of the calcium channel blocker nifedipine and the calcium channel activator BAY k 8644 were studied in anesthetized and ventilated normotensive Wistar-Kyoto (WKY) or spontaneously hypertensive rats (SHR). Both drugs were administered in a 1.5-microliter volume into the lateral ventricle of the brain (i.c.v.) or into the cisterna magna (i.c.). The injection of vehicle alone (i.c. or i.c.v.) did not significantly change mean arterial pressure (MAP) or heart rate. Nifedipine (5 and 50 micrograms/kg) and BAY k 8644 (5 and 50 micrograms/kg) induced opposite effects on MAP when centrally injected. Nifedipine decreased MAP and induced a bradycardia (i.c.v.) or no change in heart rate (i.c.), and BAY k 8644 increased MAP without any significant change in heart rate (i.c. or i.c.v.). These effects were more marked with the highest dose of either drug. These effects seemed to be of central origin, since they were suppressed by ganglionic blockade by hexamethonium (100 mg/kg i.v.), whereas after hexamethonium the hypotensive and the hypertensive responses to intravenously injected nifedipine and BAY k 8644, respectively, were preserved. Bilateral vagotomy suppressed the bradycardia induced by i.c.v. administered nifedipine. Previously i.c.v. administered nifedipine (5 micrograms/kg) antagonized the pressor response to BAY k 8644 (5 micrograms/kg i.c.v.). Changes in MAP and heart rate were significantly more marked in SHR than in WKY. These results indicate that a calcium channel inhibitor and a calcium channel activator can modulate in opposite fashion central mechanisms involved in blood pressure control.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1987

Systolic hypertension in patients with arteriosclerosis obliterans of the lower limbs.

Intraarterial blood pressure, brachial artery compliance and diameter, and pulse wave velocity were determined in 20 patients with arteriosclerosis obliterans of the lower limbs (AOD) in comparison with 10 age- and sex-matched controls. With the same mean arterial pressure as in controls, patients with AOD exhibited a significant increase in systolic pressure and decrease in diastolic pressure, resulting in an increase in pulse pressure. While brachial artery diameter and pulse wave velocity remained nearly within the normal range, arterial compliance was significantly reduced and was negatively correlated with the level of pulse pressure. The study provided evidence that: atherosclerotic modifications in patients with AOD are associated with an increase in pulse pressure, which predominates on the increase in mean arterial pressure, increased pulse pressure is related to decreased arterial compliance, which reflects intrinsic modifications of the viscoelastic properties of the arterial wall.

Adult↗