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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study was designed to evaluate the frequency of an increase in the urinary albumin excretion rate (UAER) and the factors involved in this parameter in non-diabetic obese patients; 122 non-diabetic obese patients were investigated. None had proteinuria or history of nephropathy or uropathy. Fourty of them had moderate hypertension. Compared with a group of 22 lean controls, UAER was significantly higher in the obese patients (19.0 +/- 2.0 (SEM) mg/24 h vs 3.2 +/- 0.6 mg/24 h, p < 0.001). UAER was elevated (> 20 mg/24 h) in 29 patients (23.7%). Prevalence of microalbuminuria was not significantly different in hypertensive than in normotensive patients. However UAER was significantly higher in the 32 patients with a family history of hypertension (29.6 +/- 6.3 mg/24 h vs 15.3 +/- 1.5 mg/24 h, p < 0.002). In patients with microalbuminuria, body weight was significantly higher (100.3 +/- 3.9 kg vs 91.8 +/- 1.9 kg, p < 0.05), plasma albumin was significantly lower (38.3 +/- 0.6 g/l vs 40.3 +/- 0.3 g/l, p < 0.005) and the estimated value of fractional albumin clearance was significantly higher. These results show the high frequency of microalbuminuria in non-diabetic obese patients. They suggest that UAER level may be an index of family hypertension in obese patients and that microalbuminuria is part of a widespread abnormality of the capillary permeability.
Arch Mal Coeur Vaiss 1992 Aug
PMID:[Microalbuminuria and hypertension in obese patients]. 148 58

In order to assess the relationships between increased cellular sodium-proton (Na+/H+) exchange and cardiovascular abnormalities in essential hypertension (EH), 21 young subjects as part of an ongoing longitudinal study were tested for the platelets Na+/H+ exchange using the amiloride sensitive sodium dependent component of platelet volume change under cytoplasmic acidification induced by a sodium propionate medium; cell volumes were determined by electronic cell sizing (Livne et al., Lancet 1987; i: 533-6). 24 normal subjects with normotension and without familial history of hypertension were taken as controls. Data of ambulatory blood pressure recording (ABPR) defined 2 groups according to the presence of normotension (group I, n = 10), or of hypertension (group II, n = 11): established (n = 2) or borderline (n = 9) hypertension. Hypertensive subjects (group II) had increased values of Na+/H+ exchange (k coefficient, mean (SEM): 0.287 (0.07) vs 0.228 (0.05) in control group (p less than 0.01). Na+/H+ rates were significantly related to ABPR data (r = 0.46, p less than 0.02 with diastolic charge during ABPR), but not to left ventricular mass index in g/m2 by echocardiography. Increased rates of platelets Na+/H+ exchange which were related to diastolic blood pressure levels by ABPR, and perhaps to the level of peripheric vascular resistances, may play a significant role in the development of EH in the early stages.
Arch Mal Coeur Vaiss 1991 Aug
PMID:[Results of the evaluation of platelet sodium-proton exchange in the young hypertensive subject]. 165 45

Two dopamine receptors are present on the renal vasculature: post-synaptic D1-receptors and neuronal D2-receptors. The existence of postsynaptic vascular D2-receptors is now under discussion. The aim of this study was to characterize in vitro the renal vascular response to bromocriptine, a D2 preferential agonist. Bromocriptine (10(-7) to 3.10(-5) M) induced a concentration dependent relaxation (EC50 = 1.4 +/- 0.1 x 10(-6) M, m +/- SEM, n = 5) on the isolated perfused rat kidney whose vascular tone had been previously increased by 25% with prostaglandin F2 alpha and adrenoceptors blocked (phenoxybenzamine 10(-5) M, sotalol 10(-5) M). Response to bromocriptine was comparable to that induced by dopamine on terms of EC50 and Emax (87 +/- 3% reversion of the increase in renal vascular resistance induced by prostaglandin F2 alpha). Nevertheless, unlike response to dopamine, bromocriptine-induced relaxation was not antagonized by the selective D1-receptor antagonist, SCH 23390 (3 x 10(-9) M) but was inhibited by selective D2-receptor antagonists, domperidone (10(-8) M) and DO 710 (3 x 10(-8) M). To account for renal vasodilatation, an interaction of bromocriptine with 5-HT receptors was excluded. Indeed, neither 8-OHDPAT, 5-methoxytryptamine nor 5-HT were able to induce any renal vasodilatation on the isolated perfused rat kidney and domperidone is devoid of antagonist activity on 5-HT receptors. The present results suggest that bromocriptine-induced vasodilatation on the rat renal vascular bed was linked to an interaction with vascular postsynaptic D2-receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1991 Aug
PMID:[Do renal vascular D2 receptors exist?]. 195 69

The glycoprotein complex GPIIb-IIIa of the platelet membrane and CD18 of the monocyte membrane have been established as being the central figure for the adhesion processes of the corresponding cells. The molecular structure of these 2 GPs bears some similarities. It was proposed recently that LFA-1 and Mo-1 (CD18 family) and GPIIb-IIIa might be encoded by the same gene. For this purpose, we studied the expression of Mo-1, Mo-2 (as control) receptors on monocytes and GPIIIa and GPIIb-IIIa on platelets of two GT patients as compared to normal healthy subjects. Monoclonal antibodies anti Mo-1, MO-2, AP-3 and AP-2 were used to measure the expression of the respective antigens by indirect immunofluorescence procedure. The fluorescence of the labelled cells was analysed with an Ortho Cytofluorograph 50-H. The resulting Mean Fluorescence Intensity (MFI) values of AP-2 and AP-3 showed that the patients had a total absence of GPIIb-IIIa antigens. However, Mo-1, as well as those of control Mo-2, in patients (MO-1: 672 and 716; Mo-2: 453 and 637) were similar to that of normal subjects (Mo-1: 735 +/- 74; Mo-2: 585 +/- 35; mean +/- SEM). Therefore, the normal expression of Mo-1 receptors on the monocytes of Glanzmann's thrombasthenia patients suggests different genomic regulations for Mo-1 antigens on the monocyte and GPIIb-IIIa complex on the platelet.
J Mal Vasc 1991
PMID:Normal expression of the adhesive structure Mo-1 on monocytes from patients with Glanzmann's thrombasthenia. 201 Jul 2

The influence of the parasympathetic nervous system on the cardiovascular response to a synthetic atrial peptide (atriopeptin III) was examined in conscious normotensive rats utilizing the technique of radiolabelled microspheres. Atriopeptin III was infused intravenously for 30 min at a rate of 1 microgram/min in rats pretreated with a bolus intravenous injection of atropine, 150 micrograms (n = 8), or of its vehicle (n = 8). Additional animals (n = 9) received the vehicle of both atropine and atriopeptin III. The atrial peptide decreased mean blood pressure to similar extent in rats pretreated with atropine (from 124 +/- 4.5 to 108 +/- 5.3 mmHg, mean +/- SEM, p less than 0.05) and in the controls (from 123 +/- 3.8 to 105 +/- 3.8 mmHg, p less than 0.05). Heart rate rose significantly after administration of atropine. After the 30 minute infusion, cardiac index was significantly lower (p less than 0.05) in both groups infused with atriopeptin III (23.4 +/- 2.3 after atropine pretreatment and 25.1 +/- 2.2 ml/min X 100 g without atropine) than in the group of rats given only the vehicle of both atropine and atriopeptin III (32.4 +/- 2.8 ml/min X 100 g). There was no significant difference in regional blood flow distribution within the three groups of rats. These data therefore indicate that in conscious rats atriopeptin III reduces blood pressure and cardiac output without concomitantly modifying regional blood flow distribution. They also suggest that the parasympathetic nervous system does not contribute to the hemodynamic response to atriopeptin III.
Arch Mal Coeur Vaiss 1986 Jun
PMID:[Absence of a role for the parasympathetic nervous system in the hemodynamic response to atriopeptin III in the normotensive rat]. 294 71

This study investigate the effects of Nicardipine treatment on regression of left ventricular hypertrophy (LVH), coronary hemodynamic and myocardial mechanical performance. 30 Sprague-Dawley male rats were divided into 3 groups: sham operated rats control group (SHC), untreated hypertensive rats group (RHR-U), treated hypertensive rats group (RHR-N). Systemic and coronary hemodynamics were determined by using left atrial injection of radioactive microspheres, 16 weeks after clipping. Mechanical performance was measured on isolated papillary muscle from the same animal. Results (mean +/- SEM) (Table: see text). Nicardipine treatment (10 to 15 mg intraperitoneal dosage during 8 weeks), led to: an efficient but incomplete control of hypertension. a reduction of left ventricular mass in proportion lesser than pressure decrease. a raise of coronary blood flow at rest with inversion of flow distribution between endocardium an epicardium. a decrease of "maximal" coronary blood flow. a reversal of impaired myocardial mechanical parameters towards control values except for contraction timing parameters. Decrease of "maximal" coronary blood flow could have deleterious effects on cardiac function.
Arch Mal Coeur Vaiss 1988 Jun
PMID:[Effects of nicardipine on left ventricular hypertrophy of the rat with renovascular arterial hypertension]. 297 1

The effects of a single oral dose of enalapril (20 mg) on blood pressure (BP), heart rate (HR) plasma renin activity (PRA) aldosterone (PA), converting enzyme inhibition (CEI) and enalaprilat (E, active metabolite) were investigated during 96 h in 3 groups of 5 hypertensive patients with (1) normal renal function (creatinine clearance: Clcr greater than 80 ml.min-1); (2) moderate chronic renal failure: 80 greater than or equal to Clcr greater than 30 ml.min-1; (3) severe chronic renal failure: 30 greater than or equal to Clcr greater than 10 ml.min-1. Results are as follows (mean +/- SEM): (Table: see text) CEmax: maximal plasma concentration; TEmax: delay corresponding to CEmax; TE 1/2: plasma elimination half-life; AUCE: area under plasma level versus time curve. a: p less than 0.01; b: p less than 0.001; versus (1). In the 3 groups, CEI reached 87-94% as early as the 3rd h; however, at 96 h, CE1 was higher in (3) than in (1) and (2): 77.6 +/- 3.3% versus 6.0 +/- 1.6 and 17.7 +/- 4.8 (p less than 0.001 respectively). In (3). PRA increased at the 1st h and remained elevated: at 96 h, delta PRA was + 3.0 +/- 2.9 ng.ml-1 -.h-1 in (3) versus + 0.10 +/- 0.06 and + 0.25 +/- 0.17 ng.ml-1.h-1 .n (1) and (2) [(3) versus (1): p less than 0.01]; delta PA was lower in (3): -4.56 +/- 2.01 ng. 100 ml-1 versus -0.54 +/- 0.31 and -2.50 +/- 0.38 ng. 100 ml-1 [(3) versus (1): p less than 0.05].(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1986 Jun
PMID:[Clinical pharmacology of enalapril in hypertension with chronic renal failure]. 302 74

Circulating phenolsulfotransferase M and P and monoamine oxidase activities were determined in 18 untreated essential hypertensive patients and in 35 normotensive healthy controls. Phenolsulfotransferase M is involved in the sulfoconjugation of catecholamines and their metabolites while PST P preferentially sulfates phenolic substrates. After lysis of whole blood, enzymatic activities were determined by radioenzymatic techniques using as substrates 3-methoxy-4-phenoxyphenylglycol for PST M, phenol for PST P and [14C] beta-phenylethylamine for MAO. Blood MAO activity measured by this method is fully accounted for by platelet MAO-B activity. Concerning blood PST activities, no significant difference was found in hypertensive patients compared to normotensive controls (PST M: 1.69 +/- 0.17 versus 1.66 +/- 0.08 nmoles of MHPG-sulfate/ml of blood/hour; PST P: 0.36 +/- 0.05 versus 0.27 +/- 0.04 nmoles of phenol-sulfate/ml of blood/hour). MAO activity was higher in women than in men. Significantly lower MAO B activities were observed in hypertensive patients both in men (19.25 +/- 2.20, n = 8 versus 24.35 +/- 2.22, n = 14, desaminated beta-phenyl-ethylamine/10(9) platelets/hour, x +/- SEM, p less than 0.05) and in women (23.92 +/- 2.74, n = 10 versus 35.76 +/- 2.35, n = 21, p less than 0.01) when compared to normotensive controls of the same sex. Recent in vitro studies have suggested that a reduction in platelet MAO B activity may be induced by an alteration in the phospholipidic and/or calcium environment of the enzyme. Low MAO activity in other tissues such as liver or vascular endothelium could contribute to the high sympathetic tone observed in these patients.
Arch Mal Coeur Vaiss 1987 Jun
PMID:[Blood phenolsulfotransferase and monoamine oxidase-B activity in essential arterial hypertension]. 311 77

The role of circulating bradykinin in the regulation of cardiovascular homeostasis was studied in the normotensive conscious rat using a competitive antagonist of bradykinin at the receptor level. This antagonist (B4162) was administered intravenously as a bolus dose of 400 micrograms. This dose was shown to effectively block the hypotensive effect of exogenous bradykinin (2.5 micrograms) for at least 5 min. The bradykinin antagonist was administered at the end of an infusion of angiotensin II (1 ng/min, n = 5, or 12.5 ng/min, n = 6), of methoxamine (0.5 micrograms/min, n = 5, or 4 micrograms/min, n = 6), of lysine vasopressin (0.25 mUI/min, n = 11) or of saline (10 microliter/min, n = 7). The bradykinin antagonist did not change the mean arterial pressure of the control rats. The low doses of angiotensin II and of methoxamine did not have an effect on mean blood pressure. The bradykinin antagonist however increased mean blood pressure of these rats within 1 min by 10 +/- 2 (p less than 0.01, mean +/- SEM) and by 12 +/- 3 (p less than 0.01) mmHg, respectively. The large dose of angiotensin II raised mean blood pressure from 127 +/- 3.6 to 142 +/- 4.9 mmHg and that of methoxamine from 130 +/- 2 to 146 +/- 5 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1987 Jun
PMID:[Attenuation of the vasopressor effect of angiotensin II, vasopressin and alpha 1-adrenergic stimulation by bradykinin]. 311 81

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)
Arch Mal Coeur Vaiss 1988 Jun
PMID:[Flow-dependent vasodilation of the brachial artery in the normotensive and essential hypertensive patient]. 314 33


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