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We have observed effects of acute hyperinsulinaemia on arterial pressure of five diabetics and tested the reproducibility of this action. Systolic (TAS) and diastolic (TAD) arterial pressure were studied during two hyperinsulinaemic-euglycaemic clamps effected with Artificial Pancreas (Biostator CGIIS, Miles) at one month of interval. During the first clamp, between the beginning of insulin infusion and the end of 4th stage, we have observed a fall of TAS (115 +/- 4, VS 137 +/- 6 mmHg; moy +/- SEM; p less than 0.05) and in less degree of TAD (76 +/- 2, VS 86 +/- 4 mmHg; NS). These modifications of arterial pressure were associated with no changes of heart rate and urinary sodium flow. On the other hand, we have observed a fall of serum levels of sodium (139 +/- 1, VS 141 +/- 1 mEq/l; p less than 0.05), urea (0.20 +/- 0.01, VS 0.32 +/- 0.02 g/l; p less than 0.001) whereas, balance-sheet of water was positive (+445 +/- 338 ml) at the end of clamp. During the second clamp, the fall of pressure has been reproducible, relating to the TAS (123 +/- 5, VS 145 +/- 4 mmHg; p less than 0.01) and non significantly to the TAD (78 +/- 2, VS 88 +/- 5 mmHg; NS). During the two tests, the mean of tension fall was identical (22 +/- 6 mmHg during first clamp, 22 +/- 4 mmHg during second one). So, acute hyperinsulinaemia induces a fall of arterial pressure, probably in bringing an influence on arterial vasodilatation since heart rate and urinary sodium excretion are unchanged and water balance-sheet is positive.(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1988 Jun
PMID:[Influence of acute hyperinsulinism on arterial pressure of diabetics. Reproducibility of the hypotensive effect]. 314 34

The vasoconstrictive effect of alpha-adrenoceptor agonists was studied on isolated perfused kidney from normal Wistar rats. Methoxamine (ED50 = 1.61 +/- 0.16 X 10(-6) M; m +/- SEM), phenylephrine (2.33 +/- 0.16 X 10(-6) M) and alpha-methylnoradrenaline (1.60 +/- 0.40 X 10(-6) M) acted as full agonists. Dopamine (9.5 +/- 1.08 X 10(-5) M) had a partial agonistic effect. Clonidine and B-HT 920 were inactive up to the concentration of 10(-4) M. Prazosin, but not yohimbine (10(-6) M) antagonized the response to phenylephrine (pA2 = 8.48 +/- 0.12) and to alpha-methylnoradrenaline (8.02 +/- 0.10). Our results suggest that the postsynaptic alpha-adrenoceptors which when stimulated increases vascular resistance of isolated rat kidney, belong exclusively to the alpha 1-subtype.
Arch Mal Coeur Vaiss 1984 Oct
PMID:[Characterization of the alpha adrenoreceptors in the vascular bed of the isolated rat kidney]. 615 27

To gain a better understanding of the therapeutic effect of HTA, the present study reports a new method essentially based on the non invasive non ambulatory monitoring of blood pressure by the Dinamap 845. This apparatus was initially assayed towards the measure of invasive blood pressure and by the auscultatory method, and afterwards towards the analysis of approximately one hundred resulting data. The computer analysis of the data was performed using a microcomputer which gives the results as: time dependent curves over 24 hr; histograms, percentage of the values of HTA (above 140 mmHg for the systolic and 90 mmHg for the diastolic one); numeric data such as: average values, SEM... The method reported here appears to be convenient to follow new therapeutic treatment because the data obtained before and after treatment proved to be more rigorous and less varying upon the physician. This kind of investigation seems also helpful in the case of both hypertensive emergencies and treatment of those HTA which are difficult to stabilize. But it is thought to be not easily applied to all the hypertensions studied in the usual medical practise.
Arch Mal Coeur Vaiss 1982 Jun
PMID:[Automatic non-ambulatory measurement of arterial pressure. Computer data-analysis of the evaluation of antihypertensive treatment]. 681 Aug 14

Plasma renin activity (PRA), plasma aldosterone (PA) and plasma catecholamines were measured in 3 groups of women with pregnancy of 20-38 weeks: group I of 16 normotensive controls, group II of 17 women with rest responding hypertension (RRH) and group III of 18 women with permanent hypertension (PH) (supine blood pressure greater than 140-90 mmHg after 8 days of rest, disappearing after delivery). Studies were realized on fasting ambulatory women on a normal salt diet. PRA (mean +/- SEM) was significantly higher in the RRH group than in the control and PH groups (15,8 +/- 2,3 ng/ml/h versus 6,7 +/- 0,5 and 8,9 +/- 0,9). PA was higher but not significantly in the RRH group (736 +/- 122 versus 533 +/- 52 and 502 +/- 103 pg/ml). Plasma epinephrine (PE) and norepinephrine (PNE) were significantly higher in the PH than in the control and RRH groups. 135 +/- 28 pg/nl versus 56 +/- 13 and 63 +/- 17 for PE and 387 +/- 91 versus 206 +/- 32 and 200 +/- 47 pg/ml). These data suggest that PH is linked with activation of the adrenergic system whereas RRH is linked with activation of the RAA system.
Arch Mal Coeur Vaiss 1982 Jun
PMID:[The renin-angiotensin-aldosterone system and the adrenergic system in normal pregnancy and hypertension induced by pregnancy]. 681 Aug 37

We examined renal sodium handling in rats with Hymann nephritis (HEN), an immunologically mediated model of nephrotic syndrome. Rats were studied 9-14 days following i.p. injection of anti-Fx1A antiserum. We previously demonstrated that HEN had a blunted volume expansion natriuresis (2% body weight isotonic saline infused over 5 min), excreting sodium at only half the rate of normal controls (CTL) despite similar increase in plasma atrial natriuretic peptide (ANP) concentration. Urinary excretion of cGMP accumulation by isolate glomeruli and inner medullary collecting duct (IMCD) cells in response to increasing concentration of ANP, and RNP (also called urodilatin). Results (fmol/mg prot/10 min) are means +/- SEM: [table: see text]. Basal accumulation of cGMP was not different among the groups, HEN rats hd reduced cGMP accumulation in response to ANP, and RNP. In binding studies using 125I-ANP, no difference in either density or affinity was found between CTL and HEN rats. Thus, there is a renal resistance to ANP in rats with HEN, which can be extended to other agents acting through the cGMP pathway. This resistance is not due to impaired binding of ANP, but to impaired accumulation of cGMP in responsive tissues, reflecting perhaps increased cGMP catabolism by phosphodiesterase. Such an observation may account for the altered sodium handling in nephrotic rats.
Arch Mal Coeur Vaiss 1994 Aug
PMID:[Resistance to the action of atrial natriuretic peptide and urodilatin in Heymann nephritis in vitro]. 775 73

In order to study the efficiency of individual training programs at the ventilatory threshold level, twenty COPD patients were randomized into two groups and studied over a two-month period. At the start, during, and at the end of the study all subjects performed incremental exercise tests. The trained group (59.60 SEM +/- 2.75 years) walked four times a week at the heart rate corresponding to the metabolic level of ventilatory threshold. The other group served as controls (58.2 +/- 1.80 years). A marked increase in the symptom-limited oxygen consumption (+/- 25%) (p < 0.01), the maximal ventilation (+20%) (p < 0.01), and the ventilatory threshold (+19%) (p < 0.05) was found in the trained group. No modification was recorded in the control group. The ventilatory pattern at submaximal intensities expressed in percentage of the initial oxygen consumption showed significant differences between groups, the trained-group ventilation decreased at 50% and 75% VO2 sl (p < 0.05). The breathing frequency also decreased at 50% and 75% VO2 sl (p > 0.05). Moreover, we observed an increase in the oxygen pulse at 50% VO2 sl (p < 0.05). In conclusion, this study demonstrates that individualized training at the ventilatory threshold level increases exercise tolerance and produces better ventilatory comfort in COPD patients.
Rev Mal Respir 1994
PMID:[Value of individualized rehabilitation at the ventilatory threshold level in moderately severe chronic obstructive pulmonary disease]. 781 93

Several epidemiological and experimental studies suggest that essential arterial hypertension is associated with hyperinsulinism and insulin resistance in obese subjects and also in subjects with normal body weight. Undernutrition remains frequent in adult Vietnamese people and mean body mass index is around 18.5 kg/m2 in Vietnam. The aim of this study was to look for insulin resistance in hypertensive Vietnamese subjects, despite a markedly lower BMI in Vietnam than in occidental countries. One hundred and eight hypertensive patients (51 men and 57 women) over 40 years (mean = 65.4 years) were compared with 36 healthy subjects (23 men and 13 women) over 40 years (mean = 63.8 years). Hypertensive patients had significantly higher BMI (20.5 +/- 0.3 (SEM) kg/m2 vs 18.4 +/- 0.4 kg/m2; p < 0.01), thicker triceps skinfold (1.26 +/- 0.07 cm vs 0.71 +/- 0.07 cm; p < 0.001) and not significantly different waist/hip ratio (0.88 +/- 0.01 vs 0.85 +/- 0.01). Blood glucose at fasting and 2 hours after 75 g glucose taken orally were similar in hypertensive and normotensive subjects. Plasma insulin at fasting and 2 hours after glucose were significantly higher in hypertensive patients (44.4 +/- 5.1 pmol/L vs 21.6 +/- 3.2 pmol/L; p < 0.05 and 271.1 +/- 21.6 pmol/L vs 139.1 +/- 15.2 pmol/L; p < 0.001). Thus, despite under-nutrition, hypertensive Vietnamese patients have a moderate but significant increase in BMI and fat mass without predominant abdominal localization, and a state of insulin-resistance, compared with normotensive healthy subjects.
Arch Mal Coeur Vaiss 1997 Aug
PMID:[Insulin resistance and essential hypertension in Vietnamese subjects]. 940 24

In previous studies, we demonstrated that in ANG II-treated rats, prevention of cardiac hypertrophy (CH) by enalapril was blunted by bradykinin (BK) blockade by Hoe140. The putative role of BK was assessed by chronic exogenous BK infusion and in 46 male Sprague-Dawley rats infused with ANG II. ANG II (200 ng/kg/min) alone and associated with BK at low (BKlow, 15 ng/kg/day), mid (BKmid, 100 ng/kg/day) and high doses (BKhigh, 100 ng/kg/min) were delivered by Alzet osmotic pumps for 10 days and compared to control animals (Veh). Values of systolic arterial pressure (SAP, mmHg) in conscious rats and heart weight (HW, mg/g bw) at the end of the study are reported below. Results were submitted to ANOVA and are expressed as mean +/- SEM.
Arch Mal Coeur Vaiss 1998 Aug
PMID:[Effect of chronic bradykinin infusion on angiotensin II hypertension in rats]. 974 60

This study was to assess the role of different components of the extracellular matrix (ECM) on the mobilization of Cai++ induced by angiotensin II in vascular smooth muscle cells (VSMC) from hypertensive (SHR) and normotensive (WKY) rats. The effect of AII (10-6 M) on Cai++ release was studied in VSMC isolated from the aorta of 5-week-old WKY and SHR using fluorescent imaging microscopy (fura-2). Cai++ mobilization was characterized by amplitude, slope of Cai++ increase and total amount of Cai++. Cells were cultured on glass coverslips (control) or coated with either collagen I, collagen IV, vitronectin, fibronectin and extracellular matrix (ECM) and studied at confluence between passage 3 and 9. A significant increase of Cai++ released by AII has been observed with cells from WKY cultured on collagen I (meam +/- SEM, amplitude: 192 +/- 12% of control values, slope: 194 +/- 13%, total amount Cai++: 173 +/- 12%, n = 270, p < or = 0.0001 for each, unpaired t-test). Conversely, response with SHR was not significatively modified. Cai++ mobilization was not significatively modified after culture of VSMC from SHR and WKY on collagen IV. A significative decrease of the slope (WKY: 66 +/- 6%, p < or = 0.0001; SHR: 83 +/- 5%, p < or = 0.03) and of the amount of Cai++ (WKY: 74 +/- 7%, p < or = 0.01; SHR: 74 +/- 5%, p < or = 0.01) has been observed after culture of VSMC from the 2 strains on vitronectin. A decrease in amplitude (53 +/- 3%, p < or = 0.0001), slope (38 +/- 4%, p < or = 0.0001) and Cai++ release (69 +/- 5%, p < or = 0.004, n = 106) has been observed in VSMC from SHR seeded on fibronectin. Conversely, in VSMC from WKY, Cai++ mobilisation has not been modified compared with control cells. Culture of VSMC from SHR on ECM induced a significative decrease of amplitude (49 +/- 2%), slope (54 +/- 4%) and Cai++ release (53 +/- 3%, p < or = 0.0001 for each, n = 122), while in WKY, ECM induced a significative stimulation of these parameters (amplitude: 157 +/- 11%, slope: 149 +/- 13% and Cai++ release: 130 +/- 9%, p < or = 0.0001 for each, n = 247). These results show that the Cai++ mobilization induced by AII is modified by the adhesion of cells to different ECM components. This suggests a modulation of the A II-associated signalling events via the focal adhesion points. Furthermore, a difference in this modulation is observed between SHR and WKY when cells are seeded on collagen I, fibronectin or ECM. These modulations of Cai++ mobilization could play a role in the regulation of growth and differentiation of cells during the development of hypertension.
Arch Mal Coeur Vaiss 1999 Aug
PMID:[Cellular adhesion to elements of the extracellular matrix in the hypertensive rat modulates the effect of angiotensin II]. 1048 64

We assessed the role of angiotensin (Ang) II type 1 receptor (AT1) and endothelin type A and B (ETA & ETB) receptor in cardiovascular hypertrophy associated with angiotensin II-induced hypertension (200 ng/kg.min s.c. for 10 or 17 days). Antagonism of AT1 receptors was obtained by oral administration of losartan (10 or 30 mg/kg.day) and blockade of ETA and ETB receptors was obtained by oral administration of bosentan (30 mg/kg.day). Losartan and bosentan were administered 24 h before and during the 10 days of angiotensin II (prevention) or they were given after the development of hypertension i.e. from day 10 to 17 of angiotensin II (treatment). Tail-cuff pressure (TCP) was measured before and at the end of the period of administration of antagonists. At the end of experiments, cross sectional area (CSA, mm2) of the carotid was measured after perfusion and fixation at 100 mmHg and heart weight index (HWI, mg/g body weight) was determined. Results are mean +/- SEM. [table: see text] In addition to its blood pressure lowering effect, both doses of losartan prevented and reversed the cardiovascular hypertrophy induced by angiotensin II. Similarly, bosentan prevented and reversed the effect of angiotensin II on cardiovascular structure independently of arterial pressure. These results indicate that the effect of angiotensin II on blood pressure, heart and carotid structure is exclusively mediated by AT1 receptors. The influence of bosentan suggests that endothelin plays an important role in local action of angiotensin II independently of blood pressure level.
Arch Mal Coeur Vaiss 2000 Aug
PMID:[Cardiac and vascular hypertrophy in hypertension due to angiotensin II. Effect of losartan and bosentan]. 1098 42


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