Origins of the "black/white" difference in blood pressure: roles of birth weight, postnatal growth, early blood pressure, and adolescent body size: the Bogalusa heart study.

Cruickshank JK, Mzayek F, Liu L, Kieltyka L, Sherwin R, Webber LS, Srinavasan SR, Berenson GS.

Tulane Center for Cardiovascular Health, Tulane University Medical Center School of Public Health, New Orleans, LA, USA. clinep man.ac.uk

BACKGROUND: The determinants of differences in blood pressure that emerge in adolescence between black Americans of predominantly African descent and white Americans of predominantly European descent are unknown. One hypothesis is related to intrauterine and early childhood growth. The role of early blood pressure itself is also unclear. We tested whether differences in birth weight and in carefully standardized subsequent measures of weight, height, and blood pressure from 0 to 4 or 5 years were related to black/white differences in blood pressure in adolescence. METHODS AND RESULTS: Two Bogalusa cohorts who had complete follow-up data on birth weights and early childhood and adolescent anthropometric and blood pressure measures were pooled. One hundred eighty-five children (48 black and 47 white boys and 41 black and 49 white girls) were followed up and studied after 15 to 17 years. Birth weights were a mean 443 and 282 g lower in black boys and girls, respectively, than in whites (P<0.001). Blood pressures in adolescence were 3.4/1.9 and 1.7/0.6 mm Hg higher, respectively, and tracked from early childhood. In regression analyses, birth weight accounted for the ethnic difference in adolescent blood pressure, which was also independently predicted, in decreasing impact order, by adolescent height, adolescent body mass index, and systolic blood pressure at 4 to 5 years and inversely by growth from 0 to 4 to 5 years. CONCLUSIONS: If these results can be replicated in larger and independent samples, they suggest that efforts to improve intrauterine growth in black infants as well as lessen weight gain in adolescence might substantially reduce excess high blood pressure/hypertension in this ethnic group.

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Triple Vasopeptidase Inhibition of Angiotensinconverting Enzyme/Neutral Endopeptidase/Endothelinconverting Enzyme Activities on the Hemodynamic Profile of Chronically Instrumented Unrestrained Conscious Spontaneously Hypertensive Rats.

Daull P, Blouin A, Sirois P, Nantel F, Jeng AY, Battistini B.

*Laval Hospital Research Center, Quebec Heart & Lung Institute, Laval University, Quebec, QC, Canada daggerIPS Pharma Inc., Institute of Pharmacology of Sherbrooke, Sherbrooke University, QC, Canada double daggerNovartis Institute for Biomedical Research, Novartis Pharmaceuticals Corporation, East Hanover, New Jersey, U.S.A.

Inhibition of the renin-angiotensin system with an angiotensin-converting enzyme inhibitor (ACEi) is an effective therapy in hypertension. Vasopeptidase inhibition was initially proposed with compounds inhibiting both angiotensin-converting enzyme and neutral endopeptidase (omapatrilat), but clinical trials revealed that reducing angiotensin II while blocking the degradation of vasodilatory peptides was not without concerns. We have previously investigated the combination of an ACEi with an endothelin-converting enzyme inhibitor (ECEi); now we add a neutral endopeptidase inhibitor (NEPi) toward triple vasopeptidase inhibition. Male spontaneously hypertensive rats were surgically implanted with a vascular catheter and treated with an ACEi (benazepril), a NEPi (CGS 24592) and an ECEi (CGS 35066) (continuous intra-arterial infusion at 1 or 5 mg/kg/day x 5 days each). After 15 days, drugs administration was stopped for 3 days. ACEi (1 mg/kg per day) reduced the mean arterial blood pressure by 8.4%. The addition of a NEPi and an ECEi at the same dose did not shown any added benefit. The mean arterial blood pressure came back to baseline upon cessation of treatment. ACEi (5 mg/kg per day) reduced the mean arterial blood pressure by 28%. The mean arterial blood pressure remained attenuated by 21% and 19% with the addition of the NEPi and the ECEi. Again, the mean arterial blood pressure rose back to 148 +/- 4 mmHg following cessation of treatment. Daily biochemical and hematological analysis of plasma did not reveal any signs of toxicity, except for a rapid elevation in K (40%) after 1 day of ACEi. Thus, angiotensin II inhibition plays a primary role in controlling the blood pressure of spontaneously hypertensive whereas additional NEPi and ECEi did not provide further benefits under the present dose combinations. The normalizing effect of the higher dose of ACEi by itself made it impossible to discriminate the role of neutral endopeptidase and endothelin-converting enzyme-modulated peptides and to further define the paradigm of triple vasopeptidase inhibition toward better control of vascular hemodynamics. Additional studies are underway.

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Determinants of cardiorenal damage progression in normotensive and never-treated hypertensive subjects.

Fesler P, Ribstein J, du Cailar G, Mimran A.

Department of Internal Medicine, Centre Hospitalier Universitaire, Montpellier, France.

Determinants of cardiorenal damage progression in normotensive and never-treated hypertensive subjects. Background. In the present longitudinal study, we attempted to identify the determinants of cardiorenal damage progression in normotensive subjects (<140/90 mm Hg) and patients with never-treated essential hypertension. Methods. Renal hemodynamics and function and cardiac morphology were evaluated by isotopic techniques and echocardiography at baseline and after a median follow-up period of 5.2 years (range 3 to 13) in 30 normotensive and 33 hypertensive subjects. Results. The results are mean +/- SD. Among normotensive subjects at baseline, 50% became hypertensive during follow-up. In the whole population, multivariate analysis showed that age was the main determinant of the progression of systolic blood pressure. The yearly change in glomerular filtration rate (GFR) was exaggerated in hypertensive when compared to normotensive subjects at baseline (-1.22 +/- 2.71 vs. 0.12 +/- 2.08 mL/min/year, respectively) (P= 0.033). In the whole population, only baseline systolic blood pressure remained correlated to the change in GFR, independently of GFR at baseline (model r(2)= 0.44) (P < 0.0001). The observed increase in albuminuria was correlated with change in blood pressure only in hypertensive subjects at baseline. Left ventricular mass (LVM) progression was significant only in men and its determinants were basal plasma aldosterone, serum uric acid, and triglyceride and change in systolic blood pressure (r(2)= 0.71) (P < 0.0001). Conclusion. In a population of untreated subjects, baseline blood pressure as well as progression of blood pressure during follow-up are the main determinants of the decline in GFR, progression of albuminuria, and LVM.

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Salt sensitivity of blood pressure in patients with psoriasis on ciclosporin therapy.

Magina S, Santos J, Coroas A, Oliveira JG, Serrao P, Soares-Da-Silva P, Resende C, Pestana M.

Department of Dermatology, Hospital S. Joao, Portugal.

Summary Background Hypertension is one of the main side-effects of long-term therapy with ciclosporin. However, the influence of salt intake on the 24-h mean blood pressure of patients with psoriasis treated with ciclosporin is not known. Objectives To evaluate, in patients with psoriasis, the sodium sensitivity of the ciclosporin-induced rise in blood pressure. Methods The 24-h ambulatory blood pressure was evaluated in 13 patients with psoriasis (age range 20-57 years) in two phases, before (phase I) and after the completion of 4 months of therapy with ciclosporin 3 mg kg(-1) daily (phase II). In both phases, the patients were studied in conditions of low sodium (LS) intake followed by a high sodium (HS) diet. Results Twenty-four-hour mean +/- SD blood pressure during LS and HS intake was, respectively, 86.3 +/- 1.6 mmHg and 85.5 +/- 1.8 mmHg during phase I, and 88.5 +/- 1.5 mmHg and 91.8 +/- 2.2 mmHg (P < 0.001 vs. phase I, HS; P < 0.05 vs. phase II, LS) during phase II. The median (interquartile range) sodium sensitivity index was greater during phase II than during phase I: - 0.0028 (- 0.0071 to 0.0009) vs. 0.0065 (- 0.0055 to 0.0258) (P < 0.02). The plasma levels and the daily urinary excretion of noradrenaline did not differ between phases I and II. Conclusions The ciclosporin-induced rise in blood pressure is sodium sensitive. It is also suggested that sympathetic activation is not involved in the pathogenesis of ciclosporin-induced rise in blood pressure.

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Racial disparities in the association of foetal growth retardation to childhood blood pressure.

Rostand SG, Cliver SP, Goldenberg RL.

Division of Nephrology, Department of Medicine, University of Alabama School of Medicine, Birmingham, AL 35294, USA.

BACKGROUND: Foetal growth retardation (FGR), defined as less than the 10th percentile of birth weight for gestational age, is reported to be an important contributor to hypertension and cardiovascular disease in children and adults, but findings are not consistent. For this reason we re-examined the role of FGR in childhood blood pressure. METHODS: We performed univariate and multivariate analyses on data gathered from 262 children, age 5 years, born to mothers at risk for pre-term delivery or FGR infant. The characteristics of the mothers and the children were evaluated using Student's t-test. Rates and proportions were compared using either chi-square or Fisher's exact test. Linear regression models evaluated the effect of birth weight and body mass index on systolic and diastolic blood pressure. Multivariate linear regression was used to model the effects of FGR, gestational age, body mass index, race, gender, maternal smoking, maternal gestational diabetes on blood pressure while adjusting for possible confounders. RESULTS: Systolic blood pressure was inversely associated with birth weight in white children while a small direct association was noted in African Americans. Body mass index was positively associated with systolic blood pressure in both groups. Multiple linear regression analyses showed FGR and early gestational age were associated with higher blood pressure in white but not African American children, accounting for a 13.2 mmHg difference between FGR and appropriate for gestational age groups. Blood pressure in African Americans was strongly affected by maternal gestational diabetes and smoking. CONCLUSIONS: Birth weight influences childhood blood pressure but the effects may vary depending on ethnic group. The relative importance of birth weight on blood pressure may depend on other prenatal and post-partum risks.

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Clinical comparison of automatic, noninvasive measurements of blood pressure in the forearm and upper arm.

Schell K, Bradley E, Bucher L, Seckel M, Lyons D, Wakai S, Bartell D, Carson E, Chichester M, Foraker T, Simpson K.

Department of Nursing, University of Delaware.

BACKGROUND: When the upper arm (area from shoulder to elbow) is inaccessible and/or a standard-sized blood pressure cuff does not fit, some healthcare workers use the forearm to measure blood pressure. OBJECTIVE: To compare automatic noninvasive measurements of blood pressure in the upper arm and forearm. METHODS: A descriptive, correlational comparison study was conducted in the emergency department of a 1071-bed teaching hospital. Subjects were 204 English-speaking patients 6 to 91 years old in medically stable condition who had entered the department on foot or by wheelchair and who had no exclusions to using their left upper extremity. A Welch Allyn Vital Signs 420 series monitor was used to measure blood pressure in the left upper arm and forearm with the subject seated and the upper arm or forearm at heart level. RESULTS: Pearson r correlation coefficients between measurements in the upper arm and forearm were 0.88 for systolic blood pressure and 0.76 for diastolic blood pressure (P < .001 for both). Mean systolic pressures, but not mean diastolic pressures, in the upper arm and forearm differed significantly (t = 2.07, P = .04). A Bland-Altman analysis indicated that the distances between the mean values and the limits of agreement for the 2 sites ranged from 15 mm Hg (mean arterial pressure) to 18.4 mm Hg (systolic pressure). CONCLUSIONS: Despite strict attention to correct cuff size and placement of the upper arm or forearm at heart level, measurements of blood pressure obtained noninvasively in the arm and forearm of seated patients in stable condition are not interchangeable.

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Distinct roles for the kidney and systemic tissues in blood pressure regulation by the renin-angiotensin system.

Crowley SD, Gurley SB, Oliverio MI, Pazmino AK, Griffiths R, Flannery PJ, Spurney RF, Kim HS, Smithies O, Le TH, Coffman TM.

Division of Nephrology, Department of Medicine, Duke University and Durham VA Medical Centers, Durham, North Carolina, USA. Department of Pathology, University of North Carolina, Chapel Hill, North Carolina, USA.

Angiotensin II, acting through type 1 angiotensin (AT(1)) receptors, has potent effects that alter renal excretory mechanisms. Control of sodium excretion by the kidney has been suggested to be the critical mechanism for blood pressure regulation by the renin-angiotensin system (RAS). However, since AT(1) receptors are ubiquitously expressed, precisely dissecting their physiological actions in individual tissue compartments including the kidney with conventional pharmacological or gene targeting experiments has been difficult. Here, we used a cross-transplantation strategy and AT(1A) receptor-deficient mice to demonstrate distinct and virtually equivalent contributions of AT(1) receptor actions in the kidney and in extrarenal tissues to determining the level of blood pressure. We demonstrate that regulation of blood pressure by extrarenal AT(1A) receptors cannot be explained by altered aldosterone generation, which suggests that AT(1) receptor actions in systemic tissues such as the vascular and/or the central nervous systems make nonredundant contributions to blood pressure regulation. We also show that interruption of the AT(1) receptor-mediated short-loop feedback in the kidney is not sufficient to explain the marked stimulation of renin production induced by global AT(1) receptor deficiency or by receptor blockade. Instead, the renin response seems to be primarily determined by renal baroreceptor mechanisms triggered by reduced blood pressure. Thus, the regulation of blood pressure by the RAS is mediated by AT(1) receptors both within and outside the kidney.

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Long-term effects of stress reduction on mortality in persons >/=55 years of age with systemic hypertension.

Schneider RH, Alexander CN, Staggers F, Rainforth M, Salerno JW, Hartz A, Arndt S, Barnes VA, Nidich SI.

Institute for Natural Medicine and Prevention, Maharishi University of Management, Fairfield, Iowa.

Psychosocial stress contributes to high blood pressure and subsequent cardiovascular morbidity and mortality. Previous controlled studies have associated decreasing stress with the Transcendental Meditation (TM) program with lower blood pressure. The objective of the present study was to evaluate, over the long term, all-cause and cause-specific mortality in older subjects who had high blood pressure and who participated in randomized controlled trials that included the TM program and other behavioral stress-decreasing interventions. Patient data were pooled from 2 published randomized controlled trials that compared TM, other behavioral interventions, and usual therapy for high blood pressure. There were 202 subjects, including 77 whites (mean age 81 years) and 125 African-American (mean age 66 years) men and women. In these studies, average baseline blood pressure was in the prehypertensive or stage I hypertension range. Follow-up of vital status and cause of death over a maximum of 18.8 years was determined from the National Death Index. Survival analysis was used to compare intervention groups on mortality rates after adjusting for study location. Mean follow-up was 7.6 +/- 3.5 years. Compared with combined controls, the TM group showed a 23% decrease in the primary outcome of all-cause mortality after maximum follow-up (relative risk 0.77, p = 0.039). Secondary analyses showed a 30% decrease in the rate of cardiovascular mortality (relative risk 0.70, p = 0.045) and a 49% decrease in the rate of mortality due to cancer (relative risk 0.49, p = 0.16) in the TM group compared with combined controls. These results suggest that a specific stress-decreasing approach used in the prevention and control of high blood pressure, such as the TM program, may contribute to decreased mortality from all causes and cardiovascular disease in older subjects who have systemic hypertension.

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