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Objective: The frequent association between the type 2 diabetes mellitus and cardio-vascular diseases suggests that metabolic factors may contribute to cardio-vascular remodeling. The aim of our study was to examine the relationships between left ventricular posterior wall thickness (LVPWT), pulse wave velocity (PWV), and the metabolic abnormalities of insulin resistance syndrome, in hypertensive patients., Methods: In 227 consecutive hypertensives, we examined the relationships between LVPWT, PWV, and metabolic factors: plasma glucose, insulin, total cholesterol, high density lipoprotein (HDL)-cholesterol, triglycerides levels as well as the homeostasis model assessment of insulin resistance (HOMA). The Pearson correlation coefficient and multiple regression analysis (including age, gender, body mass index, and 24-hour systolic blood pressure) were used as statistical tests., Results: In univariate analysis, glucose, HDL-cholesterol, and triglycerides levels were related to LVPWT (r = 0.19, p < 0.05; r = -0.26, p < 0.001; r = 0.31, p < 0.001, respectively); all metabolic variables, except HDL-cholesterol, correlated to PWV (plasma glucose r = 0.25, p < 0.001; total cholesterol r = 0.22, p < 0.01; triglycerides r = 0.20, p < 0.01; insulin r = 0.19, p < 0.01; HOMA r = 0.27; p < 0.001). In the multivariate model, plasma triglycerides remained correlated with LVPWT (beta = 0.19, p < 0.02) independently of systolic blood pressure, plasma aldosterone, and normetanephrine. Only HOMA and insulin level remained associated with PWV (beta = 0.14; beta = 0.13 respectively, p < 0.05)., Conclusions: These data suggest that among typical metabolic abnormalities of insulin resistance syndrome, plasma triglycerides, and insulin as well as degree of insulin resistance may contribute to cardiac hypertrophy and arterial stiffening independently of hemodynamic and hormonal factors.

Background: Proximal tubule (PT) angiotensinogen (AGT) is part of a tubular renin-angiotensin system (RAS) that participates in the regulation of sodium reabsorption along the entire nephron. Physiologic maneuvers affecting AGT expression in PT also affect systemic RAS. Here, we tested the hypothesis that PT AGT is regulated by increased glomerular filtration rate (GFR)., Methods: Complete unilateral nephrectomy (UNX) in mice was used to induce a sustained increase in GFR in the remaining kidney. AGT expression was monitored by quantitative reverse transcription-polymerase chain reaction (RT-PCR). AGT protein in PT was investigated by semiquantitative histology. We also measured AGT concentration in plasma and in 24-hour urine by a specific enzyme-linked immunosorbent assay (ELISA)., Results: Seven weeks after nephrectomy, UNX animals exhibited a 2-fold increase in tubular AGT mRNA (P <.001) compared with sham-operated control animals. The proportion of PT sections exhibiting AGT immunostaining was significantly increased at day 3 (P <.05), and remained elevated at seven weeks (UNX = 0.63 +/- 0.09, sham = 0.38 +/- 0.02, P <.01), revealing recruitment of AGT-producing cells along the PT. AGT excretion in final urine corrected for creatinine and kidney weight was also elevated by UNX at seven weeks (UNX = 209 +/- 42 pmol/mg/g, sham = 147 +/- 29 pmol/mg/g, P <.05), with no difference in plasma AGT between UNX and control animals., Conclusion: These observations suggest that AGT expression in PT adapts in the long-term to changes in GFR. In the UNX model, urinary AGT excretion is also elevated as a consequence of increase in net tubular flow.

Background: The observation of renin expression in connecting tubule, a segment that also expresses tissue kallikrein (KLK-1), raises two questions. Are the genes expressed in the same or in different cells of connecting tubule? Does this topography support the hypothesis that KLK-1 activates prorenin or is it more likely that it affords coordinated gene regulation?, Methods: Renin and KLK-1 were examined by immunostaining and in situ hybridization. Renin activation by KLK-1 was investigated in vitro. In vivo, excretion of prorenin and active renin was compared in mice homozygous for targeted inactivation of KLK-1 (TK(-/-)) and normal littermates (TK(+/+))., Results: Using in situ immunostaining for renin and in situ hybridization for KLK-1 mRNA, we found that connecting tubule cells expressing renin also expressed KLK-1. We confirmed in vitro activation of prorenin by KLK-1, but found no difference in the ratio of active renin to prorenin in urine of TK(-/-) and TK(+/+) animals. Compared to TK(+/+) controls, TK(-/-) mice exhibited significantly lower 24-hour excretion of prorenin (5.05 +/- 1.16 mg Ang I/hour vs. 9.39 +/- 1.96 mg Ang I/hour, P < 0.05) and active renin (1.98 +/- 0.25 mg Ang I/hour vs. 3.58 +/- 0.39 mg Ang I/hour, P < 0.05), with no difference in either urine volumes or plasma renin concentrations., Conclusion: Direct interaction between renin and KLK-1, not ruled out in vitro, is not supported in vivo. By contrast, lower excretion of active renin and prorenin in TK(-/-) compared to TK(+/+) suggest coordinated regulation of the two proteins in their participation to collecting duct function.

Unlabelled: Our goal was to study the relative influence of systolic blood pressure (SBP) and plasmatic markers of sympathetic and renin-aldosterone systems (RAS) activities to left atrial diameter (LAD), left ventricular posterior wall thickness (LVPWT) and pulse wave velocity (PWV), which reflect cardiovascular remodeling in hypertension., Methods: In 227 consecutive patients with hypertension (mean age +/- SD: 53.3 years +/- 13.4, 126 men), we measured: PWV, LAD, LVPWT, mean 24-hours SBP, plasma renin activity, and plasma aldosterone and catecholamine levels. Multiples linear regression analyses were performed to test statistical associations between hemodynamic and neurohumoral factors, and cardiovascular remodeling parameters, after adjustment for age, gender and body mass index., Results: LVPWT was positively correlated to SBP as well as to plasma aldosterone and meta-noradrenaline (p < 0.001). LAD and PWV were related to SBP but not to any of the biological variables. Moreover, LAD correlated to PWV independently of SBP (p < 0.05), whereas after SBP inclusion in the model, there was not significant correlation between LAD and LVPWT nor between LVPWT and PWV., Conclusion: In hypertension, the development of cardiac hypertrophy depends on SBP and the sympathetic and renin-aldosterone systems activities. The RAS is not involved in the PWV nor LAD modifications. Strong association between LAD and PWV suggest that left atrial enlargement, that may be considered as a marker of diastolic function, may results more from arterial stiffness than from ventricular hypertrophy.

There are many variations in blood pressure, ranging from that observed between systole and diastole (pulse pressure) to slower daily or seasonal variations. This variability has many facets, for example the simple concept of variation around the mean blood pressure and the more complex spectral, chaos or fractal analysis... Some of these concepts are still the subject of fundamental research and have no current clinical applications. Others, however, are already part of our evaluation of hypertensive patients or used as prognostic factors in cardiac failure or myocardial infarction. Blood pressure variability, either the pulse pressure or 24 hour variability, is associated with a higher incidence of cardiovascular complications. Although the causality of the relationship is uncertain, patients with the greatest variability seem to be at higher risk. In addition to this prognostic impact, the study of changes in blood pressure by spectral analysis may also provide indices of adrenergic tone or sympathovagal equilibrium which may be useful clinically. Finally, the combined study of blood pressure variability and heart rate lead to the baroreflex, the sensitivity of which integrates major risk factors such as blood pressure, age, heart rate and serum cholesterol. This baroreflex could be a useful parameter for stratification of cardiovascular risk. This has already been demonstrated in patients at high risk, such as those with cardiac failure or myocardial infarction.

Arterial stiffness is a strong determinant of cardiovascular risk. Pulse wave velocity (PWV) is an index of arterial stiffness, and its prognostic value has been repeatedly emphasized. The purpose of the present study was to assess the effect of heart rate (HR) on PWV. Twenty-two subjects with a mean age of 77.8+/-8.4 (SD) years and permanent cardiac pacing were studied. In each subject, PWV was measured at 5 different pacing frequencies in the same session (60, 70, 80, 90, 100 bpm), the order of the various frequencies being randomly determined. Furthermore, to test the reproducibility, a repeat measurement of PWV was obtained in one randomly selected frequency. Blood pressure (BP) was measured by conventional means at each pacing frequency. PWV appeared fairly reproducible because no significant difference was disclosed between the 2 measurements obtained at the same HR level (P=0.5) and both measurements were strongly correlated (r=0.87, P<0.001). No significant BP variation was observed during pacing. There was a highly significant effect of HR on PWV estimated by a one-way, within-subjects analysis of variance (P=0.01). This study demonstrates that HR is an important factor in the intraindividual variation of PWV in elderly subjects. This raises methodological concern about the measurement of this parameter. Standardizing PWV for HR level seems mandatory if one wants to interpret PWV changes in clinical trials or in the follow-up of patients.

Elements of a renin-angiotensin system expressed along the entire nephron, including angiotensinogen secreted by proximal tubule and renin expressed in connecting tubule, may participate in the regulation of sodium reabsorption at multiple sites of the nephron. The response of this tubular renin-angiotensin system to stepwise changes in dietary sodium was investigated in 2 mouse strains, the sodium-sensitive inbred C57BL/6 and the sodium-resistant CD1 outbred. Plasma angiotensinogen was not affected by sodium regimen, whereas plasma renin increased 2-fold under low sodium. In both strains, the variation in urinary parameters did not parallel the changes observed in plasma. Angiotensinogen and renin excretion were significantly higher under high sodium than under low sodium. Water deprivation, by contrast, induced significant activation in the tubular expression of angiotensinogen and renin. C57BL/6 exhibited significantly higher urinary excretion of angiotensinogen than did CD1 animals under both conditions of sodium intake. The extent to which these urinary parameters reflect systemic or tubular responses to challenges of sodium homeostasis may depend on the relative contribution of sodium restriction and volume depletion.

BP measurement by a physician may trigger a blood pressure and heart rate increase often referred to as the white coat effect. This pressure response may occur both in normotensive and hypertensive subjects. The identification of such individuals is usually not possible on a clinical basis. This identification is however important because white coat effect and permanent hypertension do not share the same prognosis, the white coat effect being associated with a low rate of cardiovascular complications. To avoid an important overestimation of the real blood pressure level due to this white coat effect, it is possible to increase the delay before blood pressure measurements (beyond 15 minutes) or to take into account measurements made by nurses. Reading may also have a favorable consequence. However, a blood pressure recording outside the office, that is an ambulatory or a home blood pressure measurement, is the only way to confirm the presence of a white coat effect. The decision to treat is based on this measurement.

At the start of the eighties, in the wake of the good results obtained with aspirin in secondary prevention, two studies were launched aimed at testing the effect of aspirin on the primary prevention of myocardial infarction. The results published in 1988 and 1989 were divergent: the study conducted by British doctors showed no benefit with aspirin, that conducted by American doctors showed a very distinct benefit concerning myocardial infarction but no advantage for cerebral vascular accidents. Besides, in both studies an additional risk of haemorrhagic cerebral vascular accident was described. Methodological reasons were the origin of these facts, but it resulted in a certain confusion as to the practical conduct to adopt. Ten years later it is much more clear after the publication of three supplementary trials. The benefits of aspirin in terms of prevention of myocardial infarction are certain and considerable, at the price of a haemorrhagic risk equally certain but moderate. On the other hand, questions remain concerning the preventive effect of aspirin on cerebral vascular accidents and also on the expected benefits in the female sex. In practice, the prescription of aspirin with the objective of primary prevention must take into account the absolute benefit which can be expected. This is a function of the individual absolute risk before treatment which therefore signifies an evaluation based on the risk factors. Only subjects exposed to a substantial risk before treatment are likely to benefit from aspirin. For the others, the risks linked with aspirin could counterbalance its preventive advantages.

Unlabelled: The localisation of aldosterone-producing adenomas (APA's) remains difficult. Indeed, CT scan may not detect small APA's while CT detected tumours do not necessarily produce aldosterone., Objective: To evaluate the value of adrenal vein catheterization (AVC) for the diagnosis of APA's and also the rates of unsuccessful procedures and complications., Patients: One-hundred-and-nine hypertensives with biological features of primary hyperaldosteronism were included. Plasma sodium, potassium, aldosterone and renin levels were obtained after one night in lying position. Aldosterone and renin levels were also measured after a one-hour walking period and after a sodium expansion with saline. All patients underwent a CT scan and AVC. For adrenal samples, the ratio of aldosterone to cortisol concentrations was calculated for both sides. Both ratios were divided by the opposite one and the higher was retained as an index of laterization (IL). For lack of a golden standard variable, we have taken as a working hypothesis that operated patients had an APA (n = 38) and the non operated ones bilateral hypereplasia (n = 71)., Results: Operated patients had a shorter history of hypertension, more frequently a left ventricular hypertrophy on ECG, and lower serum creatinine and potassium levels, along with a higher sodium level. None of these features appeared discriminant, however. Presence of a 10-mm tumour on CT scan was not significantly different between the 2 groups. Operated patients had more than a five-fold higher IL compared with that of non-operated patients. Analysis using a ROC curve showed that the value of 12 for "IL" was an acceptable operational criterium of lateralization, producing a specificity of 90%, while maintaining a sensitivity of 62%. AVC appeared most useful in case of middle-range pre-test probability of an APA being present, that is when when clinical, biological, or radiological features are not fully concordant. The rate of unsuccessful procedure and the rate of complications were low (1.8% and 3.6%, respectively)., Conclusion: With a low iatrogenicity, AVC appears helpful in indicating surgery mostly when clinical, biological, and CT scan features are not fully concordant. A value of 12 for IL appears to allow a high specificity while retaining an acceptable sensitivity.

The authors showed, in a spin-off study of SYST-EUR, that 24% of subjects with isolated systolic hypertension on conventional measurement were not hypertensive during ambulatory blood pressure monitoring. Moreover, in white coat hypertension, treatment had no effect either on the electrical signs of left ventricular hypertrophy or on the incidence of clinical events (cerebrovascular accident and global cardiovascular complications), contrary to what is observed in permanent systolic hypertension. These results raise question as to the diagnosis and treatment of isolated systolic hypertension in the elderly and prompt to a larger usage (if not systematic) of ambulatory blood pressure monitoring in this context. The importance of systolic blood pressure and pulsed pressure For different reasons, diastolic blood pressure was thought to be of greater prognostic significance, as the very large majority of clinical trials recruited on the basis of the value of their diastolic blood pressure alone demonstrate. In recent years, the importance of systolic blood pressure has been underlined in many studies and 3 trials have shown the unquestionable benefits of treatment of isolated hypertension. It would also appear that the pulse pressure, which reflects arterial compliance, has considerable prognostic value. In the absence of established manometric criteria and mostly of therapeutic trials, the practical use of the pulse pressure remains questionable. The interruption of the doxazosin arm of the ALLHAT trial The ALLHAT (Antihypertensive and Lipid Lowering Treatment to Prevent Heart Attack Trial) study showed a doubling of the morbidity from cardiac failure, a 19% excess of cerebrovascular events and 16% of angina pectoris in subjects treated with doxazosin compared with those treated with chlorthalidone. The differences in blood pressure with treatment were minimal and, a priori, unable to explain these results. Beyond the fact that alphablockers cannot be considered as first-line antihypertensive therapy, without doubt, the affirmation that lowering the blood pressure provides the same benefit irrespective of the antihypertensive agent used, probably needs to be reviewed.

White coat hypertension and the white coat effect are common clinical problems. Although they have similar names, they do not correspond to strictly identical entities. The white coat effect is an increase in blood pressure induced by the physician. It may be observed for all degrees of mean blood pressure and it is usually assessed by the difference between conventional and ambulatory blood pressure values. White coat hypertension is a qualitative status associating clinical hypertension and "normotension" outside the physician's office. In practice, the application of these definitions presents many difficulties. The usual methods of evaluating the white coat effect are a poor marker of the true effect as measured by continuous blood pressure monitoring. White coat hypertension has many definitions, both with respect to the threshold of clinical hypertension and to that of ambulatory normotension. Any attempt at evaluating the prognosis of these two conditions are faced with these considerations. However, the cardiovascular consequences which result appear to be mild and, usually, do not justify drug therapy. Their principal implications are above all diagnostic as they may lead to the erroneous assumption of severe or drug-resistant hypertension.

The field of hypertensive medicine is constantly and rapidly changing, especially with regards to treatment. In view of its high incidence and its complications, it is a major public health concern. This explains the periodic publication of national or international recommendations with the object of informing practitioners of the latest publications in a form applicable to clinical medicine. In France, the "Agence Nationale d'Accréditation et d'Evaluation en Santé" (ANAES) has recently published its recommendations for the management of hypertension. The dominant issues are the recognition of validated electronic sphygmomanometers for measuring the blood pressure in the out-patient setting, the evaluation of individual cardiovascular risk for treatment choice, the value of non-pharmacological interventions, the tailoring of antihypertensive treatment and the abandon of the concept of equal benefit of comparable blood pressure lowering irrespective of the molecule used.

Objective: The purpose of this study was to test the robustness of the measurement of left ventricle mass (LVM), using Devereux's formula, in the presence of a rapid change in left ventricular volume induced by nitroglycerin., Design: Forty-eight healthy volunteers with excellent echocardiographic recordings were included. The intrapatient variability of LVM measurement was assessed by two consecutive echocardiograms. The intraobserver reproducibility was assessed by the rereading of 19 echocardiograms by the same observer. The effects of nitroglycerin were compared with those of a placebo in a double-blind random manner on, the left ventricular internal dimension in diastole (LVIDd), the interventricular septum thickness, the posterior wall thickness and the LVM., Results: It was shown that both the intrapatient and the intraobserver reproducibility were high. Nitroglycerin induced a significant decrease in LVIDd compared with placebo (-0.21 +/- 0.24 versus 0.01 +/- 0.21 cm, respectively, P < 0.01) and a non-significant increase in wall thickness. These variations were negatively correlated with each other (r= -0.58, P< 0.01). Despite the change of ventricular dimensions, the variation of LVM induced by nitroglycerin was not significantly different from that induced by placebo (2.0 +/- 16.0 versus 4.7 +/- 17.0 g, respectively, not significant) and close to the intrapatient variability., Conclusion: This experiment failed to demonstrate any influence of a rapid variation of ventricle size on the calculation of LVM with the Penn convention and strongly supports the robustness of the method in vivo.

Fractal analysis is a new tool allowing to study the complexity of cardiovascular variability. This approach may be useful for investigating regulatory mechanisms. In fractal terms, homeostasis required an optimal organisation of complexity (beta coefficient close to 1): conversely, some pathological situations have proven to be associated with an altered organisation of fractals (beta coefficient different from 1). Our study aimed at determining if hypertension was associated with an alteration of the fractal component of blood pressure (BP) or heart rate (HR) variability. Eighty-eight subjects referred for high BP entered the study. BP was measured in ambulatory conditions by an automatic device during 24 hours (ABP). BP and HR were then recorded beat-to-beat by a Finapres and an ECG during 30 minutes at rest. The beta coefficient was obtained by coarse-graining spectral analysis from the BP and RR interval time series. This method has proven its interest for breaking down cardiovascular variability into an harmonic component and a non harmonic one, this latter containing fractal elements. Spontaneous baroreflex sensitivity was assessed by the method of sequences. The percentage of fractals contained in BP and RR signals remained relatively stable despite the increasing severity of hypertension. A significant but loose correlation was found between the beta coefficient of RR and ABP (r = 0.23, p = 0.053 with systolic ABP; r = 0.25, p = 0.03 with diastolic ABP). No correlation could be disclosed between ABP and the beta coefficient of BP. The beta coefficient of RR was significantly correlated with the spontaneous baroreflex sensitivity (-0.59, p < 0.0001). It is concluded that it is rather the complexity of HR signal than that of BP which is altered during hypertension. This may suggest that some regulatory processes are lost or less efficient. The correlation reported between the baroreflex gain and the beta coefficient of RR interval may reflect, in fact, an alteration of the parasympathetic drive. Globally, these results emphasise the importance of HR and probably cardiac output in the pathophysiology of high BP.

This experiment aimed at 1) comparing the spontaneous baroreflex sensitivity (SBRS) in Lyon genetically hypertensive (LH), normotensive (LN), and low blood pressure (LL) rats and 2) assessing some aspects of the mechanisms of its impairment in LH rats. Baroreflex was studied in control animals after an early chronic converting enzyme inhibition with perindopril and after a 4-wk infusion of ANG II in perindopril-treated rats. The SBRS was determined with a previously validated method, using statistical dependence between blood pressure (BP) and heart rate values recorded in freely moving animals. LH rats exhibited high BP, cardiac hypertrophy, and decreased SBRS (LH, 1.3 +/- 0.2; LN, 2.5 +/- 0.4; LL, 2.2 +/- 0.4 beats . min-1 . mmHg-1). Perindopril prevented the development of hypertension and cardiac hypertrophy and normalized SBRS. BP rose in LH and LL rats after ANG II infusion, but only LH rats, which developed a cardiac hypertrophy, had an impaired SBRS (LH, 1.1 +/- 0.2; LN, 2.5 +/- 0.2; LL, 2.8 +/- 0.3 beats . min-1 . mmHg-1). This impairment was partially reversed by an acute ANG II blockade with losartan. These results demonstrate that high BP does not account for the decreased SBRS in LH rats. SBRS impairment could result either from cardiac hypertrophy or from the direct effect of ANG II on the baroreflex loop.

The aim of this study was to elucidate further the precise nature of the so-called "white coat" (WC) effect. We enrolled 88 hypertensive (46 men, 42 women) and 18 normotensive (4 men, 14 women) subjects in whom beat-to-beat blood pressure (BP) and heart rate (HR) were measured with a Finapres device at rest (R period) and during conventional BP measurement (WC period). The WC effect was defined as WC period minus R period values of Finapres systolic BP. Using the same method, we also measured the BP and HR variations induced by mental stress (MS period) and by assuming the standing position (S period). Variability was estimated in the frequency domain for BP (BPV) and HR (HRV) and gave indices of the autonomic nervous system. Pulse wave velocity was taken as an index of arterial distensibility. In hypertensive subjects, the WC effect was significantly and positively correlated with the BP response to stress (0.51, P<.0001) and standing (0.63, P<.0001). An increased BPV was observed in the low-frequency band (0 to 0.150 Hz) during WC, MS, and S periods. In normotensive subjects, the WC effect was very slight and not correlated with the responses to stress and standing. In this group, the WC period was not accompanied with an increased BPV, unlike the stress and standing periods. HRV was similar in normotensives and in hypertensives: decreased, unchanged, and increased during MS, S, and WC periods, respectively. The PWV was significantly increased in the hypertensives relative to the normotensives, even in the quartile of those with the lowest BP (on average similar to that of the normotensives). This work shows that the WC effect is associated with an enhanced BP response to standing and mental stress; these three situations are characterized by an increased BPV in the low frequencies, suggesting a similar modification of the sympathovagal balance. The WC effect may entail an increased risk because it is associated with impaired arterial distensibility.

We assessed the role of the renin-angiotensin system (RAS) in Lyon genetically hypertensive (LH) and normotensive (LN) rats by measuring 1) kidney renin and prorenin contents; 2) effects of early, prolonged angiotensin-converting enzyme (ACE) inhibition on blood pressure (BP) and regional hemodynamics; and 3) acute and chronic responses to angiotensin II (ANG II) and norepinephrine (NE). At the adult age, LH rats differed from LN rats by elevated BP, left ventricle weight, and vascular resistances, especially in the kidneys, associated with lower kidney renin and prorenin contents. ACE inhibition (perindopril, 3 mg.kg-1.24 h-1 orally from 3 to 15 wk of age) suppressed the development of hypertension, cardiac hypertrophy, and the increase in renal vascular resistances. No specific hypersensitivity to ANG II could be disclosed in acute conditions. In perindopril-treated LH rats, a 4-wk infusion of ANG II (200 ng.kg-1.min-1) but not of NE (1,000 ng.kg-1.min-1) restored hypertension, mimicked the hemodynamic alterations seen in untreated LH rats, and produced a brief sodium retention. It is concluded that in LH rats, despite a low basal renin secretion, hypertension and hemodynamic abnormalities 1) are fully dependent on an active RAS and 2) may involve an enhanced sensitivity to the chronic effects of ANG II.

Epidemiological studies have contributed to our understanding of several aspects of hypertension which could not have been remarked upon by clinical medicine alone: 1) the continuous nature of the relationship between the level of hypertension and cardiovascular risk has shown that the clinical definition by criteria based on numbers is arbitrary and should be adjusted according to the context and therapeutic management; 2) the risk of high blood pressure is strongly dependent on the presence or absence of other risk factors (smoking, diabetes, serum lipids, left ventricular hypertrophy), a factor which is not sufficiently taken into account in clinical practice; 3) assessment of the absolute risk of an individual on the basis of the respective roles of the principal risk factors is a useful guide to treatment. Moreover, population studies have shown that mild increases in blood pressure, associated with a long individual risk, are responsible for a large number of cardiovascular events because of the many people affected. Preventive action on the whole population is necessary in addition to individual therapeutic intervention in the clinical setting.

This study was aimed to compare the white coat effect and the response to a mental stress. 29 subjects, referred for high blood pressure (BP) were included. Systolic BP (SBP) was recorded beat-to-beat with a Finapres device during 3 periods of at least 5 minutes: 1) rest (alone, in lying position); 2) white coat (5 measurements of BP with a standard mercury sphygmomanometer by the same physician); 3) mental stress (version for computer of the Stroop Word Color Conflict Test). A Coarse-graining spectral analysis was performed to compute the power in the low frequency band (PLF: 0-0.150 Hz) and in the high frequency band (PHF: 0.150-0.500 Hz). SBP was 142 +/- 3.7 during the rest period and increased significantly during the white coat (156.7 +/- 3.9 mmHg) and the mental stress (190.7 +/- 4.8 mmHg) periods. These rises of SBP levels were associated with a rise of PLF, significant only during mental stress (11.3 +/- 1.4, 15.7 +/- 3.7, 17.2 +/- 2.4 mmHg2/Hz, during rest, white coat and mental stress periods, respectively). Moreover, a significant correlation (r = 0.76; p < 0.0001) was found between the white coat effect (PAS "white coat"-PAS "rest") and the response to stress (PAS "stress"-PAS "rest"). This work shows that white coat effect is not a specific response but may rather represent an increased reactivity to stress. As it is associated with an increased power in the LF band like the response to stress, this white coat effect may involve an activation of the sympathetic system.

We compared the consequences of chronic angiotensin-converting enzyme (ACE) inhibition with quinapril and of specific AT1 blockade with losartan in a renin-dependent model of hypertension, the (mRen2)27 transgenic rats (TG). Animals were orally treated with 10 mg/kg/24 h of either quinapril (TGQ, n = 13) or losartan (TGL, n = 12) from age 4 to age 9 weeks. Indirect systolic blood pressure (SBP), and sodium and water balances were measured for 3 consecutive weeks. Nine-week-old rats were instrumented to record aortic BP in the conscious state. In addition, they received an infusion of glucose and saline to increase their diuresis and thus allow accurate assessment of their renal excretion during short time periods. These rats were studied for three one-h periods: (a) baseline, (b) after the administration of a bradykinin (BK) antagonist, and (c) after a cross-treatment; i.e., TGQ rats receiving losartan (10 mg/kg intravenously, i.v.) and TGL rats receiving quinapril (10 mg/kg i.v.). TGL rats differed from TGQ rats by an unconsistently lower indirect SBP associated with significantly lower urinary volume and sodium excretion, whereas the sodium balance did not differ between the two groups. In conditions of fixed sodium intake the aortic BP of TGQ rats was still nonsignificantly different from that of TGL rats, and TGQ rats also exhibited two-fold higher natriuresis. The BK antagonist had no effect in either group, whereas losartan decreased the BP of TGQ rats. We conclude that in TG rats ACE inhibition is associated with an increased natriuresis as compared with specific AT1 blockade, an effect that is independent of the sodium intake. Because a BK antagonist had no effect, such a difference might be due to an antinatriuretic effect of AT2 receptors in chronic conditions.

A 32-year-old pregnant woman with poor life and hygiene conditions presented with premature labour, fever and diarrhoea. After admission she gave birth to a stillborn child. The examination revealed a septicaemia with massive haemolysis and renal failure. Six blood cultures obtained on admission yielded Clostridium perfringens. The outcome was favourable after an adapted antibiomicrobial therapy. This case illustrates the potential severity of Clostridium perfringens foodborne toxi-infection which can lead to abortion and septicaemia with massive haemolysis.

Objective: To investigate the link between cardiac hypertrophy, elevated blood pressure level and baroreflex impairment, we assessed cardiac baroreflex function in a hypertensive model almost devoid of cardiac hypertrophy, obtained by nitric oxide synthesis inhibition., Methods: Thirteen adult male Wistar rats were treated orally with NG-nitro-L-arginine methyl ester (L-NAME, 50 mg/kg per 24 h) for 4 weeks. Fifteen control rats received tap water. At the end of the treatment aortic blood pressure was recorded continuously and the baroreceptor-heart rate curve was assessed by bolus injections of phenylephrine and sodium nitroprusside (10 different doses of each)., Results: Mean blood pressure was higher in L-NAME rats than in control rats, whereas body weight was similar. Total heart weight and left ventricular weight did not differ between the groups. Cardiac baroreflex was reset in hypertensive rats, as indicated by a rightwards shift of the mean blood pressure-heart rate curve. Its gain was decreased significantly in L-NAME rats, whereas the heart rate range was not different between the two groups., Conclusion: L-NAME hypertensive rats exhibit an original impairment of cardiac baroreflex, characterized by a range-independent decreased gain which is not due to cardiac hypertrophy.