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Biomedical subjects

S Laurent

Publications and source records attributed to S Laurent.

At least 199 records · Page 11Linked to original sources
PubMed1989

Nicardipine decreases blood pressure and heart rate at nucleus tractus solitarii of spontaneously hypertensive rats.

The effects of the dihydropyridine (DHP) calcium channel antagonist, nicardipine, on central cardiovascular regulation were investigated by injecting it into the cisterna magna or directly into the nucleus tractus solitarii (NTS), in anesthetized normotensive or spontaneously hypertensive (SHR) rats. Intracisternal injections of nicardipine (1-10 micrograms/kg) dose-dependently decreased blood pressure in SHR; there was no significant change in cardiovascular parameters in normotensive rats. In SHR, nicardipine (100 ng) microinjected bilaterally into the NTS produced hypotension and bradycardia. The same doses of nicardipine intravenously injected did not change either parameter. Previous administration of the beta-adrenoceptor blocking drug, tertatolol (50 micrograms/kg i.v.), prevented the nicardipine-induced bradycardia and hypotension after injection into the NTS. These data suggest that part of the central cardiovascular effects of nicardipine result from an interaction with DHP sites within the NTS leading to a withdrawal of the sympathetic tone.

Adrenergic beta-Antagonists↗
PubMed1989

Central cardiovascular effects of dihydropyridines in spontaneously hypertensive rats.

Intracerebroventricular (i.c.v.) injections of dihydropyridine derivatives calcium channel agonist (BAY K8644) and antagonist (nifedipine, nicardipine, PN 200-110) induced opposite long-lasting changes in blood pressure (BP) in pentobarbital anesthetized spontaneously hypertensive rats (SMR). I.c.v. nifedipine (NIF), nicardipine (NIC), and PN 200-110 decreased mean blood pressure dose-dependently and stereoselectively, (+) NIC and (+) PN being 8 and 3 times more potent than their (-) isomers, respectively. The decrease in BP was due to a withdrawal of the sympathetic tone, since NIF- and NIC-induced falls in BP were suppressed after either hexamethonium (HXM), 6 OHDA or bilateral adrenalectomy. I.c.v. BAY K8644 increased BP dose-dependently. The i.c.v. BAY K8644-induced hypertensive effect was inhibited: a), by NIF and (+) PN but not by (-) PN, therefore probably occurring at central DHP sites; b), by HXM and reserpine, thus probably mediated by an increase in sympathetic tone; c) by i.c.v. methylatropine (MA) while i.v. MA and i.c.v. HXM had no inhibitory effect, thus probably involving central muscarinic sites. In SHR, NIC did not after the K(+)-evoked ACh release but suppressed the BAY K8644-induced increase in ACh release. In anesthetized normotensive control rats (WKY), neither i.c.v. NIF, NIC or BAY increased BP and HR while, in conscious SHR it decreased BP without any change in HR. These data increased BP and HR while, in conscious SHR it decreased BP without any change in HR. These data suggest that central DHP sites may be involved in the cholinergic transmission and may participate in genetic hypertension via sympathetic tone.

Animals↗
PubMed1989

Indirect, noninvasive evaluation of pressure wave transmission in essential hypertension.

Blood pressure, carotid-femoral and brachioradial pulse wave velocities were measured in 123 male subjects: 32 normal subjects and 91 age-matched patients with sustained essential hypertension. The ratio between brachioradial (BR) and carotid-femoral (CF) pulse wave velocities was used as a marker of pressure wave amplitude changes from the aorta to the brachial artery. The ratio was similar in normotensive and hypertensive subjects and decreased with age to the same extent in both populations. In older subjects, the decrease in the ratio indicated that the amplitude of pulse pressure was quite similar in the aorta and the brachial artery whether the subjects were normotensives or hypertensives. The study provided evidence that adaptive changes occur in the arterial (aortic) wall in hypertension, for the effects of age on pressure wave transmission are similar in normal subjects and hypertensive patients. Such findings may be of prime importance in understanding the brachial blood pressure readings of patients with hypertension.

Adult↗
PubMed1989

Influence of the autonomic nervous system on brachial artery diameter and compliance in normotensive and hypertensive patients.

Based on non-invasive studies using pulsed Doppler velocimetry, it appears that the brachial artery in hypertensive humans responds actively to positional changes and norepinephrine infusion, exhibiting an abnormal constriction following norepinephrine administration and an enhanced vasodilating response when raising the legs from supine position. Such modifications occur in the absence of significant change in blood pressure and heart rate and could not be explained exclusively on the basis of high flow dilatation. It is suggested that the hypertensive brachial artery responds actively to modifications of the autonomic nervous system. Changes observed following legs raising probably involved stimulation of mecanoreceptors in the low pressure system.

Autonomic Nervous System↗
PubMed1989

[Central modulation of the baroreflex response to phenylephrine in rats. Lack of interaction between calcium channel modulators and the renin-angiotensin system].

We have previously shown that a calcium channel activator (BAY K 8644) can decrease the baroreflex control of heart rate in SHR when intracerebroventricularly (i.c.v.) administered. In pentobarbital anesthetized SHR, the inhibitory effect of BAY (3 micrograms/kg i.c.v.) on baroreflex sensitivity (BRS; ramp method: phenylephrine 2 micrograms i.v.; BAY: 0.14 +/- 0.05 vs control: 0.39 +/- 0.08 msec/mmHg; p less than 0.01) was fully suppressed after pretreatment with the muscarinic antagonist atropine methylnitrate (80 micrograms/kg i.c.v.) suggesting the involvement of cholinergic pathways in the inhibitory effect. Since A II was reported to centrally increase arterial pressure through an enhanced release of acetylcholine and to depress BRS, we tested whether the effect of BAY on BRS could involve central A II systems. The A II antagonist [Sar 1Ile8] A II (30 micrograms/kg/min i.c.v.) suppressed the inhibitory effect of A II on BRS (control: 0.32 +/- 0.09; A II: 0.10 +/- 0.02; Sar1 Ile8 + A II: 0.39 +/- 0.08 msec/mmHg) but not the inhibitory effect of BAY (3 mu g/kg i.c.v.) on BRS. These results suggest that the central inhibition of BRS by BAY unlikely involves central A II systems.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1989

Calcium-entry blockers and arterial compliance in hypertension.

Calcium-entry blockers dilate small arteries as well as large arteries, particularly in the brachial and the carotid circulations. This dilating effect is associated with an increase in systemic and brachial arterial compliance, which is poorly related to the level in blood pressure. Calcium-entry blockers are able to reverse the reduced arterial compliance observed in patients with essential hypertension, with important consequences to the structure and function of the heart and large vessels.

Arteries↗
PubMed1989

[Anomalies in the hemodynamic response to short lasting emotional stress in essential hypertensive subjects].

Systemic hemodynamics, brachial artery diameter (D) and blood flow velocity (v) were determined non-invasively in 26 normotensive subjects (NT) and 34 age- and sex-matched essential hypertensive patients (HT) using pulsed Doppler systems (4 and 8 MHz), at rest and during 2 min periods of mental arithmetic (MA) inducing reproducible changes in blood pressure. During MA in HT, v increased (from 5.3 +/- 1.1 to 8.4 +/- 1.6 cm/sec) to a greater extent (p less than 0.01) than in NT (from 4.9 +/- 0.7 to 6.3 +/- 1.4 cm/sec). Hand exclusion did not change the increase in v in HT and in NT. During MA, D did not change in both groups. Systolic and diastolic arterial pressure increased to a greater extent (p less than 0.01) in HT than in NT, while HR and pulse pressure increased to the same extent in both groups. Since cardiac output and D did not change during MA, instantaneous variations of v likely reflected modulation of arteriolar tone. These results suggest an enhanced vasodilatory response of muscle resistance vessels in HT as compared to NT. The lack of change in D suggest an increase in vascular tone of large arteries likely contributing to the rise in pulse pressure during MA in both groups.

Adult↗
PubMed1989

[Therapeutic response to canrenone of patients with essential hypertension as a function of sodium transport anomalies and ouabain sensitivity of erythrocytes].

The presence of Na+ transport abnormalities (decreased affinity of the Na+/K+ pump or the Na+, K+ cotransport for internal Na+, increased Na+:Li+ countertransport, increased Na+ leak), Na+ content, Na+/K+ pump activity and sensitivity to ouabain were investigated in erythrocytes from 13 patients with essential hypertension. According to the presence or absence of Na+ transport abnormalities, the patients were divided into two groups: TrNa(+) (n = 9) and TrNa(-) (n = 4) respectively. Compared with TrNa(-) patients, TrNa(+) patients were characterized by: (i) a higher arterial pressure (131.4 +/- 11.8 vs 110.0 +/- 13.2 mmHg, p less than 0.05), (ii) an increased erythrocyte Na+ content (8.9 +/- 1.0 vs 6.3 +/- 0.8 mmol/l.cells, p less than 0.01) associated with (iii) a decreased rate constant of Na+/K+ pump activity (235 +/- 26 vs 309 +/- 45 h-1, p less than 0.05) and (iv) a higher sensitivity to ouabain (0.76 +/- 0.23 vs 1.12 +/- 0.26 microM, p less than 0.05). Oral administration of canrenone 50 mg per day during 7 weeks decreased mean arterial pressure by 10-30 mmHg in 6 out of the 9 TrNa(+) patients. Conversely, it decreased mean arterial pressure in only one out of the 4 TrNa(-) patients. The hypotensive effect of canrenone in TrNa(+) patients was not associated with normalization of their Na+/K+ pump activity. Canrenone did not modify the sensitivity to ouabain of either the TrNa(+) or the TrNa(-) patients. Before treatment, acute injection of ouabain provoked an inhibition of the erythrocyte Na+/K+ pump, without any change in Na+ content.(ABSTRACT TRUNCATED AT 250 WORDS)

Biological Transport↗
PubMed1988

Endogenous opiate system and dihydropyridine-induced central regulation of sympathetic tone in rats.

Intracerebroventricular injections of nicardipine (10 micrograms/kg) to SHR induced hypotension which was suppressed by pretreatment with 6-OHDA. This hypotension was also inhibited by a previous injection of naloxone (100 micrograms/kg i.c.v.) whereas the hypotension induced by intravenously injected nicardipine (10 micrograms/kg) was not changed. It is suggested that the release of endogenous opioids is involved in the sympatho-inhibitory effect of centrally administered dihydropyridine calcium channel antagonists.

Animals↗
PubMed1988

Central and peripheral cardiovascular effects of the enantiomers of the calcium antagonist PN 200-110.

The negative inotropic effects and the central and peripheral hypotensive effects of (+) and (-) PN 200-110 were investigated in cultured chick heart cells and in spontaneously hypertensive rats, respectively. There was a large difference in negative inotropic potency between the two enantiomers in cultured chick embryo ventricular cells: the (+) enantiomer was 140 fold more potent (IC50 = 1.1 +/- 0.2 nM) than the (-) enantiomer (IC50 = 160 +/- 20 nM). (+) PN 200-110 was 10 fold more potent than (-) PN 200-110 in lowering blood pressure after intravenous injection and only three fold more potent after intra-cerebroventricular injection (i.c.v.) into pentobarbital-anaesthetized spontaneously hypertensive rats. I.c.v. administered (+) PN 200-110 (1 microgram/kg) partially antagonized the hypertensive response to i.c.v. administered BAY K 8644 (30 micrograms/kg), a calcium channel agonist, while the same dose of the (-) enantiomer did not change the i.c.v. BAY-induced increase in blood pressure. These results suggest that the dihydropyridine calcium channel antagonist, PN 200-110, may act centrally and stereoselectively at the level of the dihydropyridine receptor sites involved in the control of blood pressure in spontaneously hypertensive rats.

Anesthesia↗
PubMed1988

Sodium and large arteries in hypertension. Effects of indapamide.

Epidemiologic studies evaluating arterial pulse wave velocity together with blood pressure indicate that: (1) salt intake has an independent effect on arteriolar tone and arterial wall properties, with the former indirectly and the latter directly contributing to increased arterial stiffness with age; and (2) normotensive adult subjects who follow a low sodium diet have reduced arterial stiffness and this effect is independent of blood pressure. Conversely, in elderly persons with isolated systolic hypertension, isotonic saline infusion causes a predominant increase in systolic pressure due to an increase in the stiffness of the arterial wall. The diuretic indapamide produces a decrease in blood pressure without significant change in brachial artery diameter. The result indicates a shift of the pressure-diameter curve, reflecting for the first time in humans a pharmacologic effect of the drug on arterial vessel. Furthermore, diuretic drugs may increase arterial distensibility and compliance in hypertensive patients, but this effect seems to be more pronounced in older than in younger subjects. In the latter, either activation of the sympathetic nervous system or potassium depletion, or both, might counteract the improvement in arterial distensibility caused by blood pressure reduction and sodium depletion. Based on epidemiologic, clinical, and pharmacologic studies, this critical review suggests that, in patients with essential hypertension, changes of sodium intake in diet or administration of diuretics, or both, affect the status of large arteries independently of blood pressure changes.

Aging↗
PubMed1988

Central and peripheral hypotensive effects of the optical isomers of nicardipine, a dihydropyridine calcium channel antagonist, in rats.

Central and peripheral hypotensive effects of (+)- and (-)-nicardipine (1-10 micrograms/kg i.v. or i.c.v.) were investigated in normotensive and SH rats. The results suggest that a stereoselectivity exists for the peripheral and central hypotensive effects of the nicardipine isomers. (+)-Nicardipine was shown to be 3-8 times as potent as the (-) isomer in reducing blood pressure in all the experiments.

Animals↗
PubMed1988

Renal and systemic hemodynamics in borderline hypertension.

Cardiac output (CO), renal blood flow (RBF), and glomerular filtration rate were measured in 29 young patients with borderline hypertension, in comparison with 26 normotensive controls of the same age and sex. In patients with borderline hypertension, both CO and RBF were significantly increased, whereas the RBF/CO ratio remained within the normal range. No significant changes in glomerular filtration rate and renal filtration fraction were observed. The study clearly demonstrated that renal ischemia was absent in young patients with borderline hypertension.

Adolescent↗
PubMed1988

Converting enzyme inhibition and the common carotid circulation in older patients with sustained essential hypertension.

Arterial diameter, blood flow and vascular resistance of the common carotid artery were studied using a pulsed Doppler system in patients with uncomplicated sustained essential hypertension and compared with age-matched normal subjects. In hypertensive patients below the age of 45 years, arterial diameter and blood flow remained within the normal range, while vascular resistance was increased. In hypertensive patients over 45 years of age, arterial diameter was also normal, but blood flow was reduced and vascular resistance markedly increased. Thus, both small and large arteries were altered in the common carotid circulation of patients with sustained essential hypertension. Acute oral administration of converting enzyme inhibitor produced dilatation of both small (vascular resistance) and large (arterial diameter) arteries in the carotid circulation. In addition, in older patients, blood flow significantly increased and vascular resistance markedly decreased both in acute and long-term situations. Thus converting enzyme inhibition was able to reverse the abnormalities of the common carotid circulation of older subjects with sustained essential hypertension.

Adult↗
PubMed1988

Non-invasive ultrasonic study of maximal aortic blood acceleration in patients with borderline and sustained essential hypertension.

Using a pulsed Doppler method to evaluate the aortic velocity curve transcutaneously, the maximal aortic blood acceleration was evaluated in normal subjects and in age-matched patients with borderline and sustained essential hypertension. Maximal aortic blood acceleration was significantly elevated in patients with borderline hypertension and remained within the normal range in patients with sustained hypertension. Since maximal aortic blood acceleration is relatively insensitive to preload and afterload, these findings might give indirect information on the contractile state of the myocardium in patients with hypertension.

Adult↗
PubMed1988

Flow-dependent vasodilation of the brachial artery in essential hypertension: preliminary report.

Brachial artery haemodynamics including brachial artery diameter and local blood flow velocity were studied in 10 normotensive subjects and 10 age-matched hypertensive patients. A bidimensional pulsed Doppler system was used at rest, during a 2-min period of distal circulatory occlusion and during reactive hyperaemia. The kinetics of changes in blood flow velocity and brachial artery diameter were determined during successive and reproducible manoeuvres. The two parameters decreased significantly during distal artery occlusion in both groups. During reactive hyperaemia, blood velocity reached similar maximal values in both groups and brachial artery diameter increased significantly in both normotensives and hypertensives. Changes in the brachial artery diameter during reactive hyperaemia were positively and significantly correlated to changes in blood flow velocity recorded at the same level. No significant difference was found between normotensives and hypertensives. This study has provided a demonstration of velocity-dependent variations in the diameter of a large artery in humans; the results suggest that velocity-dependent vasodilation of the brachial artery is not impaired in essential hypertension.

Blood Flow Velocity↗
PubMed1988

Atrial natriuretic peptide decreases contractility of cultured heart cell: preliminary report.

We tested the hypothesis that atrial natriuretic peptide (ANP) has a direct negative inotropic effect on the cultured chick embryo ventricular cell, an experimental system devoid of endogenous neurotransmitters. At 10(-8) and 2.5 x 10(-7) mol/l ANP [rat ANP-(1-23)] significantly and reversibly decreased contractility in spontaneously beating cells. The positive inotropic effect of angiotensin II (2.5 X 10(-7) mol/l) on spontaneously beating cells was fully antagonized by ANP (2.5 X 10(-7) mol/l) and the amplitude of contraction decreased below control levels. In contrast (1) the increase in contractility in response to extracellular calcium 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) mol/l) or of the beta-adrenergic agonist isoproterenol (10(-6) mol/l) was unchanged by ANP. These results indicate that ANP-(1-23) has a direct negative inotropic effect on cultured chick heart cells and may affect intracellular messengers involved in the cardiac effects of angiotensin II.

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