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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using pulsed Doppler methods, hemodynamics of the common carotid and the brachial arteries were measured in 10 patients with essential hypertension. After vasodilatation due to Cadralazine, a Dihydralazine-like substance, mean arterial pressure significantly decreased and heart rate increased. Change in PRA was significantly and positively correlated with the change in heart rate. In the brachial artery circulation, diameter and vascular resistance decreased while blood flow velocity and volumic blood flow did not increase significantly. In the common carotid artery circulation, diameter, mean blood flow did not change. However, vascular resistance and tangential tension decreased slightly. The increase in heart rate was strongly and negatively correlated (r = 0.82 p less than 0.01) with the change in the carotid artery tangential tension (measured as the product between mean arterial pressure and arterial radius) while no comparable correlation was observed with the change in blood pressure or arterial radius alone. The study suggested that in essential hypertensives, modifications in the carotid artery tangential tension secondary to arteriolar vasodilatation contribute actively to the baroreflex response.
Arch Mal Coeur Vaiss 1986 Jun
PMID:[Non-invasive study of the role of carotid distension in the baroreflex response to the arteriolar vasodilator cadralazine in essential hypertension]. 309 14

The spontaneously hypertensive rat (SHR)--animal model for human essential hypertension--develops a generalized arteriopathy. The present paper discusses the atherogenic influence of hypertensive arterial lesions. The following changes in the intima might influence its permeability and barrier function, increase the trapping effect and stimulate the smooth muscle cell proliferation: the hyper-reactivity of endothelial cells; the decreased thickness of endothelial cell periphery; the reduced intercellular junction pathways; the increase in basal lamina and glycosaminoglycan sub-endothelial material; the mononuclear cell infiltrations; the widened fenestrae in the internal elastic lamina. Some hypertensive changes of the tunica media may also interact with atherogenic process through reduced smooth muscle cell lipolytic capabilities, slowed transmural diffusion, perturbed efflux, aggravated media hypoxia, namely: the decrease in esterase and cholinesterase activities, the activations of some lysosomal enzymes, the increase in collagen, glycosaminoglycan and elastin content; the increased media thickness and transmural passage; the modified smooth muscle cell behavior.
Arch Mal Coeur Vaiss 1986 Nov
PMID:[Hypertensive arteriopathy and atherogenesis: cellular and molecular interactions]. 310 95

The aim of this study is to evaluate the antihypertensive effect of placebo assessed by 24 hr non invasive blood pressure monitoring. 20 patients (16 males, 4 females, 55 +/- 10 years old) with primary hypertension (WHO stage I or II) were included with a diastolic blood pressure greater than or equal to 100 mmHg (mean blood pressure from three clinical readings). Casual blood pressure and blood pressure monitoring (Spacelabs - 4 measurements per hour during a 24 hr period) were established before and at the end of the placebo run in period (one placebo tablet given once daily at 8 h-8 h 30 a.m. for 15 days). Overall sample data: There was no antihypertensive effect of the placebo with casual BP (167 +/- 16-109 +/- 6 mmHg before and 167 +/- 16-109 +/- 7 mmHg after placebo) and with 24 hr B.P. monitoring (142 +/- 14-96 +/- 8 mmHg before and 141 +/- 14-96 +/- 8 mmHg after placebo). The circadian curves were similar. Individual patient data: A clinical placebo effect (B.P. decrease of at least 10 mmHg) was found in 5 patients for the systolic B.P. and in 2 for diastolic B.P. A significant ambulatory placebo effect (p less than 0.05) was found in 5 patients for the 24 hr systolic B.P. and in 4 patients for the 24 hr diastolic B.P. However, patients with clinical placebo effect were not the same as those with ambulatory placebo effect. There was no correlation between the clinical and the ambulatory response to placebo treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1987 Jun
PMID:[Study of the placebo effect in using the non-invasive ambulatory measurement of blood pressure]. 311 67

We have compared platelet and plasma catecholamines (radioenzymatic assay with catechol-O-methyl transferase) and urinary metanephrines (high performance liquid chromatography) in 16 patients with phaeochromocytoma, 12 essential hypertensives, and 15 normotensive volunteers. Hypertensive patients with or without phaeochromocytoma had labile or paroxysmal hypertension with normal or borderline blood pressures between paroxysms. Catecholamine concentrations in platelets and plasma did not differ in essential hypertensives and controls, but were higher in patients with phaeochromocytoma than in subjects without tumour, with values overlapping between groups. Metanephrine excretion was markedly higher in phaeochromocytoma than in essential hypertension, with no intergroup overlap. Platelet adrenaline plus noradrenaline content was highly correlated to urinary metanephrines (r' = 0.830, n = 28 p less than 0.01). Using as a cut-off point the highest values measured in essential hypertensives, the sensitivity of each measurement was 1.00 for metanephrines, 0.87 for platelet catecholamines and 0.50 or less for plasma catecholamines. Measurement of platelet catecholamine content is a sensitive test and an appropriate alternative to metanephrine measurement in the difficult cases of suspected phaeochromocytoma with intermittent hypertension.
Arch Mal Coeur Vaiss 1987 Jun
PMID:[Measurement of platelet catecholamine content for the diagnosis of pheochromocytoma with intermittent hypertension]. 311 76

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 non invasively using a pulsed Doppler system in 19 patients with essential hypertension and 9 normotensive subjects, before and after placebo (glucose) or increasing doses of norepinephrine (10, 20 and 40 ng/kg/min; i.v.) given in a single blind fashion. In hypertensive patients, norepinephrine (40 ng/kg/min) induced (i) a significant decrease in brachial artery diameter, local blood velocity, volumic flow and conductance and (ii) a small increase in mean arterial pressure. These hemodynamic changes did not occurred 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.
Arch Mal Coeur Vaiss 1987 Jun
PMID:[Hyperreactivity of the humeral artery to noradrenaline in essential hypertension patients]. 311 80

The acute hemodynamic effects of intravenous Nicardipine (N), a new calcium antagonist, were studied in 8 patients with moderate essential hypertension. The forearm arterial blood flow (ABF) was measured using plethysmography before and after N infusion: 1st step was obtained after infusion of 1 mg during 5 min then 1 mg during 25 min; a second step was obtained after the infusion of the same dose during the same time; thus a cumulative dosage of 4 mg was infused over a total duration of 60 mn. Systolic (SBP), diastolic (DBP) mean (MBP) blood pressure and heart rate (HR) were measured every minute using a non invasive device (Dinamap). Systemic vascular resistances (SVR) were calculated. Plasma concentration of N was determined at the beginning, in the middle and at the end of each step. Results are as follows: (table; see text) A 33% decrease in SVR was observed at the 2nd step whereas MBP decreased by 15% only. The date confirm the potent vasodilatory effect of intravenous N at low dosage; the BP alteration was moderate in relation to an increase in local blood flow. These results indicate that Nicardipine could be useful as part of the treatment of chronic arteriopathy and Raynaud disease.
Arch Mal Coeur Vaiss 1987 Jun
PMID:[Acute hemodynamic study of intravenous nicardipine in arterial hypertension]. 311 83

In arterial hypertension, hyperviscosity with hemorheological disturbances and platelet dysfunction may play a role in the prognosis and complications of the disease. We studied the effects of Nicardipine (NIC) on these blood disturbances in a group of 21 untreated patients with essential hypertension, aged 25 to 70 years (SBP/DBP = 185 +/- 28/105 +/- 17 mmHg). During one hour before and 4 hours after the IV injection of single doses of 5, 7.5 or 10 mg NIC over 5 min, blood pressure was recorded automatically (Dinamap). Hemorheological variables and platelet function were studied before and 30 min, 3 h and 24 hours after the injection. NIC lowered blood pressure and increased heart rate significantly (At 5 min, SBP = -24 mmHg; DBP = -18 mmHg; HR = +22 b/min). These effects were dose-dependent with rapid onset and short duration (less than 2 hrs). NIC decreased plasma viscosity from 1.36 +/- 0.08 to 1.30 +/- 0.07 Cst; p less than 0.01, whole blood viscosity from 22.4 +/- 2.8 to 20.7 +/- 1.5 mPas; p less than 0.05 for gamma = 0.512 s-1, and erythrocyte filterability with the Ca++ ionophore A 23187 from 16.3 +/- 3.8 to 13.5 +/- 3.1; p less than 0.01. Platelet aggregation with ADP was unchanged, but aggregation with A 23187 decreased from 46.9 +/- 21.2 to 31.3 +/- 25.6; p less than 0.05, as well as plasma levels of beta-thromboglobulin (71.2 +/- 29.8 to 55.4 +/- 24.3 ng/ml; p less than 0.02) and platelet generated malonaldehyde (7.2 +/- 1.8 to 6.7 +/- 1.4 nM/10(9) platelets; NS).(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1987 Jun
PMID:[Effects of intravenous nicardipine on blood pressure, hemorheology platelet function in arterial hypertension. Dose-effect relations]. 311 84

Calcium channel blocking agents are considered to be particularly effective in reducing blood pressure (BP) in low renin essential hypertension and in primary aldosteronism. The aim of this study was to compare the acute BP response to nicardipine in 2 opposite situations of stimulation of the renin angiotensin system: eight patients (49 +/- 13 years, mean arterial BP (MAP) 123 +/- 8 mmHg) with primary aldosteronism (active renin less than 5 pg/ml, group 1) and nine patients (38 +/- 17 years, MAP: 107 +/- 13 mmHg) with renovascular hypertension and high level of active renin (greater than 25 pg/ml, group 2). They had not taken any antihypertensive treatment since at least one week. After 60 minutes in the supine position (T0) nicardipine was infused at a rate of 7.5 mg/h during 10 minutes (T10), 15 mg/h from the 10th to 20th minute (T20) and 30 mg/h during the last ten minutes (T30). Thus, a total cumulative dose of 8.75 mg was administrated in 30 minutes. BP was recorded by an indirect oscillometric method (Sentrom) every 2 minutes and renin was assayed through an immuno-radiometric procedure (IRMA). There was an important and similar BP fall in the 2 groups (Gr 1: T10-6 p. 100, T20-17 p. 100, T30-25 p. 100; Gr 2: T10-7 p. 100, T20-13 p. 100, T30-18 p. 100) with a very significant dose-effect relation (r = 0.67, p less than 0.001). There was also an important increase in heart rate similar in the 2 groups (+35 p. 100, +25 p. 100, ns).(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1988 Jun
PMID:[Acute response to calcium inhibitors in secondary arterial hypertension: does renin play a role?]. 314 97

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).
Arch Mal Coeur Vaiss 1988 Jun
PMID:[Pulse wave velocity and ambulatory blood pressure in essential arterial hypertension]. 314 13

Three groups of 11 male subjects with the same mean age were studied: normotensives (group I), patients with sustained essential hypertension (group II) and patients with borderline hypertension (group III). M-mode echocardiography provided a measure of aortic root systolic diameter (D) and left ventricular mass index (LVMi, g/m2). We have used a 4 MHz pulsed doppler velocity meter with spectral analysis to measure instantaneous ascending aortic blood velocity. Measurements values were averaged during 10 s and included: stroke volume (SV, cm3 = integrated velocity over one cardiac cycle.aortic cross sectional area (3.14D2/4)), cardiac output (CO, cm3 = SV.heart rate), systemic vascular resistance (SVR, mmHg/cm3.s-1 = MAP/co) and maximal aortic acceleration (MA, cm/s2). (Table: see text). Stroke volume and cardiac output were similar in three groups. SVR was higher in group II than in group I. The myocardial contractility appreciated from the maximal aortic acceleration (Bennett et al, Cardiovasc Res 1984; 18: 632-8) was increased in patients with borderline hypertension and remained within the normal range in patients with sustained essential hypertension despite and increase in cardiac mass.
Arch Mal Coeur Vaiss 1988 Jun
PMID:[Non-invasive measurement by Doppler pulse of cardiac output and maximal aortic acceleration in essential arterial hypertension]. 314 28


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