Renal resistive index and low-grade inflammation in patients with essential hypertension.

In essential hypertension, increased renal resistive index (RRI) is associated to a reduction of renal function and microalbuminuria, and to renal tubulo-interstitial damage. A tubulo-interstitial inflammatory infiltration was found in experimental models of hypertension, and serum high-sensitive C-reactive protein (hsCRP) levels correlated with urinary markers of tubulo-interstitial damage in humans. We studied the relationship between RRI and serum hsCRP in hypertensives with preserved renal function, without microalbuminuria. We investigated hypertensive patients without diabetes, renal failure, microalbuminuria or major inflammatory disease. Serum levels of hsCRP were assayed. RRI was calculated by intrarenal Doppler ultrasound and considered pathologic when ≥0.70 or >95% of upper confidence limit expected for age decade. The renal volume-to-resistive index ratio (RV/RRI) was also calculated. We evaluated 85 patients (57±14 years, 61 males). Patients with pathologic RRI (n=21) were older and had significantly higher hsCRP levels (4.70±2.30 vs 2.93±2.09 mg l(-1), P<0.01) compared with patients with normal RRI, as well as patients with decreased RV/RRI (n=43). HsCRP was directly related with RRI (r=0.41, P<0.001) and inversely with RV/RRI (r=-0.35, P<0.001). HsCRP proved to be a significant predictor of both pathologic RRI and decreased RV/RRI, even after adjustment. In essential hypertension low-grade inflammation is associated with tubulo-interstitial damage evaluated by Doppler ultrasonography.

Impairment of cardiopulmonary receptor sensitivity in the early phase of heart failure.

OBJECTIVES: To characterise the efficiency of the cardiopulmonary baroreflex system in the early phase of heart failure and its relation to limitation of physical activity. DESIGN: Forearm blood flow (venous occlusion plethysmography), vascular resistance, and central venous pressure (CVP), estimated from an antecubital vein, were measured in the supine position at baseline and 15 minutes after application of lower body negative pressure at -7 and -14 mm Hg (receptor downloading) or leg raising (receptor loading). SUBJECTS: Heart failure patients without limitation (NYHA class I; n = 18) or with slight limitation of physical activity (NYHA class II; n = 13), and 11 healthy controls. RESULTS: The efficiency of the cardiopulmonary baroreflex function, expressed by the slope of the relation between CVP changes and the corresponding changes of calculated forearm vascular resistance (gain), was reduced both in NYHA class I patients (mean (SD) -1.99 (0.83) v -2.78 (0.66) in controls; p < 0.05) and NYHA class II patients (-1.29 (0.5); p<0.001 v controls). However, change in peripheral vascular resistance during preload increase was similar in controls (-3.3 (0.9) units) and in NYHA class I patients (-3.3 (2.1) units; NS v controls), and was significantly reduced only in NYHA class II patients (-1.6 (1.3) units, p < 0.03 v controls). The gain in the cardiopulmonary reflex was related to the distance walked during the six minute corridor test. CONCLUSIONS: A reduced tonic efficacy of the cardiopulmonary reflex system is already detectable in the early phase of heart failure, the impairment in acute response to preload increase being detectable only in symptomatic patients.

Increased cardiac sympathetic activity and insulin-like growth factor-I formation are associated with physiological hypertrophy in athletes.

Physiological hypertrophy represents the adaptive changes of the heart required for supporting the increased hemodynamic load in regularly trained healthy subjects. Mechanisms responsible for the athlete's hypertrophy still remain unknown. In 15 trained competitive soccer players and in 15 healthy men not engaged in sporting activities (sedentary control subjects) of equivalent age, we investigated the relationship among cardiac growth factor formation, cardiac sympathetic activity, and left ventricular morphology and function. Cardiac formation of insulin-like growth factor (IGF)-I, endothelin (ET)-1, big ET-1, and angiotensin (Ang) II was investigated at rest by measuring artery-coronary sinus concentration gradients. Cardiac sympathetic activity was studied by [(3)H]norepinephrine (NE) kinetics. Cardiac IGF-I, but not ET-1, big ET-1, and Ang II, formation was higher in athletes than in control subjects (P<0.01). NE levels in arterial and peripheral venous blood did not differ between groups. In contrast, coronary sinus NE concentration was higher in athletes than in control subjects (P<0.01). Cardiac, but not total systemic, NE spillover was also increased in athletes (P<0.01), whereas cardiac [(3)H]NE reuptake and clearance were not different. Echocardiographic modifications indicated a volume overload-induced hypertrophy associated with increased myocardial contractility. Multivariate stepwise analysis selected left ventricular mass index as the most predictive independent variable for cardiac IGF-I formation and velocity of circumferential fiber shortening for cardiac NE spillover. In conclusion, increased cardiac IGF-I formation and enhanced sympathetic activity selectively confined to the heart appear to be responsible for the physiological hypertrophy in athletes performing predominantly isotonic exercise.

Cardiac angiotensin II formation in the clinical course of heart failure and its relationship with left ventricular function.

In 76 patients with heart failure (HF) (New York Heart Association [NYHA] classes I through IV) and in 15 control subjects, cardiac angiotensin II (Ang II) generation and its relationship with left ventricular function were investigated by measuring aorta-coronary sinus concentration gradients of endogenous angiotensins and in a part of patients by studying (125)I-labeled Ang I kinetics. Gene expression and cellular localization of the cardiac renin-angiotensin system components, the density of AT(1) and AT(2) on membranes and isolated myocytes, and the capacity of isolated myocytes for synthesizing the hypertrophying growth factors insulin-like growth factor-I (IGF-I) and endothelin (ET)-1 were also investigated on 22 HF explanted hearts (NYHA classes III and IV) and 7 nonfailing (NF) donor hearts. Ang II generation increased with progression of HF, and end-systolic wall stress was the only independent predictor of Ang II formation. Angiotensinogen and angiotensin-converting enzyme mRNA levels were elevated in HF hearts, whereas chymase levels were not, and mRNAs were almost exclusively expressed on nonmyocyte cells. Ang II was immunohistochemically detectable both on myocytes and interstitial cells. Binding studies showed that AT(1) density on failing myocytes did not differ from that of NF myocytes, with preserved AT(1)/AT(2) ratio. Conversely, AT(1) density was lower in failing membranes than in NF ones. Ang II induced IGF-I and ET-1 synthesis by isolated NF myocytes, whereas failing myocytes were unable to respond to Ang II stimulation. This study demonstrates that (1) the clinical course of HF is associated with progressive increase in cardiac Ang II formation, (2) AT(1) density does not change on failing myocytes, and (3) failing myocytes are unable to synthesize IGF-I and ET-1 in response to Ang II stimulation.

Renal endothelin in heart failure and its relation to sodium excretion.

BACKGROUND: Recent studies have shown that endothelin-1 (ET-1) antagonists increase sodium excretion and improve renal blood flow in experimental heart failure (HF). However, despite a number of investigations that have reported a significant increase in ET-1 plasma levels in patients with HF, it is still not known whether increased renal synthesis and urinary excretion of ET-1 occur. Our aim was to investigate renal ET-1 formation and its relation to sodium excretion in patients with HF. METHODS: One hundred forty-seven patients with HF, subdivided according to New York Heart Association (NYHA) functional classes, and 28 healthy controls were studied. ET-1 and big ET-1 were measured in plasma and in 24-hour urine by radioimmunoassay. Atrial and brain natriuretic peptide, arginine vasopressin, plasma renin activity, and hemodynamic variables were also investigated. RESULTS: Urinary ET-1 excretion was already increased in NYHA class II patients (P <.001 vs controls), whereas plasma ET-1 increased only in NYHA class III and IV patients (P <.001). In the 71 subjects who were not receiving diuretic treatment, urinary ET-1 was selected as the strongest predictor of sodium excretion by multivariate stepwise analysis. CONCLUSIONS: Urinary ET-1 excretion increases in an earlier phase of HF than plasma ET-1 and appears to be closely correlated with sodium excretion, indicating renal ET-1 is a target for ET-1 antagonists in patients with HF.

Early sequence of cardiac adaptations and growth factor formation in pressure- and volume-overload hypertrophy.

To investigate the time sequence of cardiac growth factor formation, echocardiographic and hemodynamic measurements were performed at scheduled times, and mRNAs for angiotensinogen, prepro-endothelin-1 (ppET-1), and insulin-like growth factor I (IGF-I) were quantified with RT-PCR and localized with in situ hybridization in pigs (fluothane anesthesia) by use of pressure or volume overload (aortic banding and aorta-cava fistula, respectively). Relative peptide formation was also measured by radioimmunoassay. In pressure overload, angiotensinogen and ppET-1 mRNA overexpression on myocytes (13 times vs. sham at 3 h and 112 times at 6 h, respectively) was followed by recovery (12 h) of initially decreased (0.5-6 h) myocardial contractility. In volume overload, contractility was not decreased, the angiotensinogen gene was slightly upregulated at 6 h (6.7 times), and ppET-1 was not overexpressed. IGF-I mRNA was overexpressed on myocytes (at 24 h) in both volume and pressure overload (14 times and 37 times, respectively). In the latter setting, a second ppET-1 overexpression was detectable on myocytes at 7 days. In conclusion, acute cardiac adaptation responses involve different growth factor activation over time in pressure versus volume overload; growth factors initially support myocardial contractility and thereafter induce myocardial hypertrophy.

Selective upregulation of cardiac endothelin system in patients with ischemic but not idiopathic dilated cardiomyopathy: endothelin-1 system in the human failing heart.

Only scarce information is available on the activity and modifications of the cardiac endothelin (ET)-1 system in heart failure due to ischemic (ICM) or idiopathic dilated (DCM) cardiomyopathy. The activity of the ET-1 system was investigated by measuring cardiac ET-1 and big ET-1 formation and quantifying cardiac mRNA for prepro-ET-1 (ppET-1), ET-converting enzyme-1, and ET(A) and ET(B) receptors both in myocardium and in isolated myocytes using Northern blot, reverse transcription-polymerase chain reaction, and in situ hybridization in 22 patients with DCM and 20 with ICM who underwent cardiac transplantation and in 7 potential heart transplant donors (nonfailing hearts). Notwithstanding a similar increase of plasma ET-1 in the 2 groups, cardiac ET formation, mRNA levels for ppET-1, and ET(A) and ET(B) receptors were higher on both the myocardium and isolated myocytes from ICM than on those from DCM hearts (P<0.001 for all). ppET-1 and ET-converting enzyme-1 mRNAs were expressed on myocytes and endothelial and interstitial cells in ICM, whereas in DCM and nonfailing hearts they were mainly expressed on nonmyocyte cells. In both ICM and DCM, the ET(A) mRNA signal was expressed on both myocytes and nonmyocyte cells, whereas ET(B) mRNA was almost exclusively localized on nonmyocyte cells. ET(A)- and ET(B)-specific receptor binding was increased on both myocytes and cardiac membranes, showing a positive correlation with left ventricular ejection fraction in ICM (r=0.78 and 0.70) but not in DCM patients. The present results show that human ventricular myocytes express all of the components of the ET-1 system, which is selectively upregulated in ICM patients and appears to be functionally important in the maintenance of cardiac function.

Endothelin-1 urinary excretion, but not endothelin-1 plasma concentration, is increased in renovascular hypertension.

Animal experiments have shown an increase in prepro-endothelin-1 (prepro-ET-1) mRNA expression in the clipped kidney but none in the aortic and mesenteric arteries in 2-kidney, 1-clip Goldblatt hypertensive rats. The present study was aimed at investigating whether plasma and renal endothelin-1 (ET-1) systems are differently activated in patients with renovascular hypertension (RH). The plasma concentration and urinary excretion of ET-1 were measured in 5 patients with RH (before and after successful renal angioplasty), in 7 patients with essential hypertension (EH), and in 8 normotensive control subjects. Immediately before renal angioplasty, plasma samples for ET-1 and plasma renin activity (PRA) measurements were withdrawn from the aorta and both renal veins. Unlike the PRA, the plasma ET-1 concentration did not significantly differ between the involved and the uninvolved sides. The urinary ET-1 excretion level (Fig 1) was markedly increased in patients with RH (30+/-4 ng/g urinary creatinine (UC) vs. 2.5+/-0.2 ng/g UC and 2.6+/-0.5 ng/g UC in control subjects and patients with EH, respectively; P<.001), whereas the plasma ET-1 concentration was normal (0.8+/-0.2 pg/mL vs. 0.65+/-0.3 pg/mL and 0.8+/-0.2 pg/mL in control subjects and EH, respectively, not significant). Renal angioplasty was followed in all patients by normalization of blood pressure and PRA. One week after angioplasty, urinary ET-1 decreased to one fourth of baseline (8.04+/-5.23 ng/g UC, P<.001 vs. values before angioplasty and P<.04 vs. control subjects) and normalized 1 month thereafter (3.13+/-1.62 ng/g UC, not significant vs. control subjects), whereas plasma ET-1 remained steady. The present findings clearly indicate that in patients with RH, urinary ET-1 excretion is increased, whereas plasma ET-1 concentration remains normal. Successful percutaneous transluminal renal angioplasty induced a notable reduction in ET-1 urinary excretion, whereas it did not affect ET-1 plasma concentration.

Cardiac growth factors in human hypertrophy. Relations with myocardial contractility and wall stress.

The aim of the present study was to investigate whether and which cardiac growth factors are involved in human hypertrophy, whether growth factor synthesis is influenced by overload type and/or by the adequacy of the hypertrophy, and the relationships between cardiac growth factor formation and ventricular function. Cardiac growth factor formation was assessed by measuring aorta-coronary sinus concentration gradient in patients with isolated aortic stenosis (n=26) or regurgitation (n=15) and controls (n=12). Gene expression and cellular localization was investigated in ventricular biopsies using reverse transcriptase-polymerase chain reaction and in situ hybridization. Cardiac hypertrophy with end-systolic wall stress <90 kdyne/cm2 was associated with a selective increased formation of insulin-like growth factor (IGF)-I in aortic regurgitation and of IGF-I and endothelin (ET)-1 in aortic stenosis. mRNA levels for IGF-I and preproET-1 were elevated and mainly expressed in cardiomyocytes. At stepwise analysis, IGF-I formation was correlated to the mean velocity of circumferential fiber shortening (r=0.86, P<0.001) and ET-1 formation to relative wall thickness (r=0.82, P<0. 001). When end-systolic wall stress was >90 kdyne/cm2, IGF-I and ET-1 synthesis by cardiomyocytes was no longer detectable, and only angiotensin (Ang) II was generated, regardless of the type of overload. The mRNA level for angiotensinogen was high, and the mRNA was exclusively expressed in the interstitial cells. Ang II formation was positively correlated to end-systolic stress (r=0.89, P<0.001) and end-diastolic stress (r=0.84, P<0.001). Multivariate stepwise analysis selected end-systolic stress as the most predictive variable and left ventricular end-diastolic pressure as the independent variable for Ang II formation (r=0.93, P<0.001). In conclusion, the present results indicate that the course of human left ventricular hypertrophy is characterized by the participation of different cardiac growth factors that are selectively related both to the type of hemodynamic overload and to ventricular function.

Peripheral vascular resistance limits exercise functional capacity of mild hypertensives.

To evaluate the physiological basis for suboptimal peak exercise oxygen consumption (VO2p) observed in the early stage of hypertension, 25 WHO Stage I hypertensive men with normal left ventricular mass and 10 healthy control subjects of equivalent age underwent the maximal cardiopulmonary exercise test with contemporary measurement of cardiac output with Tc99m angiocardiography. At peak exercise hypertensive patients had lower VO2p (p < 0.045) and cardiac output (p < 0.014) and higher vascular resistance (p < 0.010) than controls. At multiple regression analysis VO2 was positively related to cardiac output in controls (r = 0.80, p < 0.02), whereas in hypertensives the best (negative) correlation was observed with peripheral vascular resistance (r = -0.72, p < 0.04). Thus reduced cardiopulmonary function during physical exercise in hypertensives seems to be mainly related to impaired peripheral vascular autoregulation.

Increased renal endothelin formation is associated with sodium retention and increased free water clearance.

To investigate whether renal endothelin (ET)-1 participates in water and sodium handling, we investigated the influence of different sodium intakes on renal production of ET-1 in eight healthy subjects. The functional relationship with the renin-angiotensin system was also studied. Renal ET-1 formation is affected by sodium intake, because 1 wk of high sodium decreased urinary ET-1 excretion (-34%, P < 0.05), whereas a low-sodium diet increased ET-1 excretion (66%, P < 0.05) and mRNA expression for preproendothelin-1 in epithelial cells of medullary collecting ducts and endothelial cells of the peritubular capillary network. Increased ET-1 renal synthesis was associated with sodium retention and increased free water clearance. Urinary ET-1 excretion changes from normal to low-sodium diet were negatively related to contemporary changes in sodium excretion (r = 0.97, P < 0.05) and were positively correlated with free water clearance (r = 0.97, P < 0.05). These correlations were maintained during angiotensin-converting enzyme inhibition, which only partially reduced ET-1 renal excretion. These results indicate that renal ET-1 production is indeed modulated by varying sodium intakes and may exert a role in sodium and water handling.

Both plasma and renal endothelin-1 participate in the acute cardiovascular response to exercise.

Plasma endothelin (ET-1) and renal endothelin are two distinct functional systems involved in maintaining blood volume. To investigate whether plasma and renal ET-1 participate in the cardiovascular response to exercise-induced hypovolaemia, we studied changes in plasma and urinary ET-1 in healthy non-professional athletes after 2 h of jogging performed both without and with drinking isotonic fluids. After the run, which caused a 13% plasma volume (PV) reduction, plasma and renal ET-1 (+117% and +118%) increased significantly (all P < 0.01). Fluid loss restitution during the run significantly attenuated either the PV contraction (-1.2%) and plasma and renal ET-1 increase (+2 and +3%). At multiple regression analysis changes in AVP plasma concentration, and not in PRA or PV per se, were significantly related to ET-1 changes both in plasma and urine. The present findings indicate that both plasma and renal ET-1 participate in the cardiovascular response to hypovolaemia induced by long-lasting, dynamic exercise.

Relationship of renin-angiotensin system and ET-1 system activation in long-lasting response to postural changes.

The present study was performed in seven healthy subjects (aged 22-35 years) to investigate 1) whether plasma and urinary endothelin-1 (ET-1) are involved in the response to postural changes and 2) the relationship between ET-1 formation and the renin-angiotensin system (RAS). Six hours of standing caused a prompt but very short-lasting increase in plasma ET-1 concentration (59% after 5 min, 12% after 1 h) and a notable and sustained enhancement of urinary ET-1 excretion (from 0.59 +/- 0.10 to 1.43 +/- 0.28 pg/min, or 142%; P < 0.001). Plasma renin activity increased by 169% after 1 h of standing. A parallel contraction of urinary volume (-62%), sodium excretion (-55%), and free water reabsorption (-24%) occurred. The return to the supine position after 6 h of orthostasis caused a reduction to baseline values of the ET-1 urinary excretion and urinary volume within 2 h. Inhibition of angiotensin-converting enzyme blunted, but did not eliminate, the orthostasis-induced increase in ET-1 urinary excretion (100%, P < 0.002) and changes in the renal functions. The present results indicate that renal ET-1 is involved in the hemodynamic long-lasting responses to postural changes and that its increase is partially controlled by RAS and suggest that ET-1 might play a role in the regulation of renal function in humans.

Clinical evaluation of the QuietTrak blood pressure recorder according to the protocol of the British Hypertension Society.

METHODS: The QuietTrak ambulatory blood pressure recorder (Tycos-Welch-Allyn, Arden, North Carolina, USA) was evaluated according to the protocol of the British Hypertension Society (BHS). QuietTrak, a lightweight (355 g), automatic, programmable device, uses an auscultatory measuring system. The protocol of the BHS was composed of subsequent phases with QuietTrak and two observers taking simultaneous measurements on the same arm. RESULTS: No interdevice differences were observed at analysis of variance test either before or after a 1-month period of routine clinical use. The average difference between mercury sphygmomanometer and QuietTrak for systolic and diastolic blood pressures was -0.6+/-3.6 and -0.4+/- 3.6 mmHg before and -0.7+/- 3.3 mmHg and 0.6+/- 3.8 mmHg after the 1-month use. At the main static device validation procedure, performed in 85 subjects, the average difference between observers and QuietTrak was -0.3+/- 3.4 and 0.1+/- 3.5 mmHg for systolic and diastolic blood pressures. Eighty-nine per cent and 99% of systolic and 88% and 98% of diastolic QuietTrak readings were within 5 and 10 mmHg of obsevers, determinations (Class A). In children (n = 33) 87% of systolic and 90% of diastolic QuietTrak readings differed by less than 5 mmHg from the observers' readings (average difference -1.1+/-3.9 and 0.1+/- 3.6 mmHg, respectively). In the elderly (n = 30), 95% and 92% of systolic and diastolic readings were within 5 mmHg of mercury column determinations (average difference -0.8+/-3.2 and -0.2+/-4.5 mmHg). In pregnancy (n = 30), 93% of systolic and 100% of diastolic readings were within 5 mmHg of mercury column determination (average difference -0.3+/-3.4 and 0.1+/- 2.9 mmHg). Device reliability was not affected by posture. Ninety-six per cent and 89% of systolic and diastolic readings differed by less than 5 mmHg from the mercury column determinations in the supine position, 90% and 90% in the standing position, and 88% and 90% in the sitting position. During the treadmill exercise (Bruce protocol), 69% and 88% of systolic and 56% and 83% of diastolic QuietTrak readings differed by less than 5 and 10 mmHg from the observers' measurements. CONCLUSION: The QuietTrak achieved A rating for systolic blood pressure and A rating for diastolic blood pressure according to the criteria of the BHS protocol. The device was acceptable to patients because of its small size, light weight and noiseless performance.

Plasma endothelin and renal endothelin are two distinct systems involved in volume homeostasis.

This study of seven healthy young subjects was designed both to establish whether endothelin-1 (ET-1) is involved in the homeostasis of blood volume and to clarify the relationship between plasma and urinary ET-1. Acute volume expansion (+17%) caused increases in venous blood pressure (+4.4 mmHg) and the plasma concentration of ET-1 (+129%) and a decrease (-99%) in the urinary excretion of ET-1. Volume depletion (-8.5%) provoked an increase in the plasma concentration of ET-1 without altering the urinary excretion of ET-1. Passive elevation of an arm resulting in a local decrease of venous blood pressure (-17 mmHg) elicited an increase of the local formation of ET-1, with a 10-fold increase in the venous-arterial gradient compared with the opposite arm, which lay at the level of the heart. The increased local formation of ET-1 was blunted by volume expansion. The results indicate that 1) plasma ET-1 and urinary ET-1 represent two different endothelin-generating systems, both of which are involved in the regulation of blood volume, and 2) plasma ET-1 appears to be an important mechanism for the long-lasting adaptations of venous wall tension to changes in blood volume.

Increased number of thromboxane A2-prostaglandin H2 platelet receptors in active unstable angina and causative role of enhanced thrombin formation.

The current study was designed to investigate the number and affinity of platelet thromboxane A2/prostaglandin H2 (TxA2/PGH2) receptors in patients with unstable angina and, if any, the role played by the increased thrombin formation that is a common finding in these patients. Measurements taken during active unstable angina but not those taken during inactive angina showed an increase number (p < 0.001), without changes in affinity, of platelet TxA2/PGH2 receptors, evaluated as the binding capacity of iodine 125-PTA-OH, a stable TxA2 analogue. Moreover patients with active angina had higher plasma concentrations of fibrinopeptide A (FPA) (p < 0.0001), which were significantly related to the number of platelet TxA2/PGH2 receptors (r = 0.76; p < 0.01). Heparin infusion but not aspirin treatment promptly normalized the number of TxA2/PGH2 receptors and significantly reduced plasma FPA concentrations. In an in-vitro study thrombin in a concentration similar to that found in vivo significantly increased the number of platelet TxA2/PGH2 receptors (p < 0.01), whereas heparin did not affect TxA2/PGH2 receptors. These results have important therapeutic implications and indicate the preferential use of heparin rather than aspirin during the acute phase of unstable angina.

Twenty-four-hour blood pressure changes in young Somalian blacks after migration to Italy.

Blood pressure changes induced by migration from Somalia to Italy were studied in 25 normotensive clinical healthy blacks (aged 29 +/- 6 years) who had immigrated from Mogadishu to Florence. Basal and 24-h ambulatory blood pressure, venous compliance, and daily urinary electrolyte excretion were measured on arrival and 6 months later. After 6 months both basal pressure (P < .05 for systolic blood pressure, P < .01 for diastolic blood pressure) and 24-h blood pressure (P < .004 for systolic blood pressure, P < .01 for diastolic blood pressure) had significantly increased. Urinary sodium excretion had also increased (P < .001), whereas plasma renin activity was significantly reduced (P < .05). The ambulatory pressure increase was significantly related to the urinary sodium increase (r = 0.49; P < .01). At follow-up 8 of 25 blacks were hypertensive according to the WHO definition (basal diastolic blood pressure > 90 mm Hg). In conclusion, an increase in 24-h blood pressure is detectable after immigration and changes seems to be mainly related to higher sodium intake in the Western diet.

Comparison of ambulatory blood pressure monitoring and conventional office measurement in the workers of a chemical company.

The aim of the present study was to define the different prevalence of hypertension when conventional office measurement and ambulatory monitoring are performed in a population of unselected workers. All the workers of a Florentine chemical company were invited to participate in the study. Enrolled subjects underwent blood pressure measurement using a conventional sphygmomanometer and ambulatory blood pressure monitoring. Of 191 workers, 145 agreed to participate in the study (76%). Six of the 145 were excluded from further analysis because they were undergoing antihypertensive therapy. Confidence limits for ambulatory monitoring were defined at 95% on normotensive workers. Thirty-five (25%) workers were found to be hypertensive according to World Health Organization parameters (diastolic pressure > 90 mmHg) but only 14 of the 35 had higher 24-h diastolic ambulatory blood pressure than the 95% confidence limits of controls.

Changes in blood pressure reactivity and 24-hour blood pressure profile occurring at puberty.

To evaluate blood pressure reactivity in children and its changes in adolescents, the acute pressor response to a video-game stress test and the noninvasive ambulatory blood pressure monitoring were evaluated in 62 healthy children divided into three age groups. Basal blood pressure values were measured according to the NIH Task Force. With baseline measures and body mass index controlled for, analysis of covariance showed that the video game provoked significant and incremental cardiovascular reactivity across the games in adolescents when compared with the two other groups of children. The same group of children showed also a significantly higher systolic ambulatory pressure during the daytime, whereas no significant difference was observed by basal BP measurement. In conclusion an increased reactivity to external stimuli was observed in adolescents, and this pattern was strictly associated with a higher daily blood pressure.