Lean Hypertensive Subjects Research Articles

Cardiovascular and sympathetic responses to a mental stress task in young patients with hypertension and/or obesity.

Present study was aimed to investigate sympathetic responses to mental stress with hypothesis that the presence of obesity in patients with hypertension has a modifying effect. Young male subjects, 8 with hypertension grade I, with BMI 25 kg/m(2) (HT), 10 with hypertension grade I, and BMI 30 kg/m(2) (HT OB), 14 healthy controls with BMI 30 kg/m(2) (OB), and 13 healthy controls with BMI 25 kg/m(2) (C) underwent the Stroop test. ECG was recorded continuously to evaluate heart rate variability (HRV). Blood pressure (BP) and catecholamine concentrations were measured at baseline, at the end of mental stress test and 15 min thereafter. Patients with HT demonstrated increased adrenaline concentrations and enhanced stress-induced noradrenaline release compared to that in healthy controls. In obese subjects, stress-induced increase of systolicBP was lower compared to lean individuals. Stress exposure induced a significant rise in the low frequency power component of HRV, however the increase was lower in the HT OB group compared to C. Obesity in patients with hypertension did not lead to a different reaction in comparison with lean hypertensive subjects. The present data demonstrate higher sympathoadrenal activity in early-stage of hypertension. Obesity is connected with higher resting systolicBP and modifies the HRV response to mental stress.

Correlation Between Plasma Leptin and Endotelin-1 Plasma Level in Obese Hypertensive Subjects

Background . Hypertension is frequently found in obesity, although the mechanisms for obesity related hypertension are still unclear. Several studies showed the role of endothelin-1 in the development of hypertension associated with obesity. More recent studies showed the possibility for the role of leptin in obesity related hypertension. In vitro study with human umbilical vein endothelial cells (HUVECs) showed correlation between leptin and endothelin-1. The aim of this study was to clarify the relationship between leptin, body mass index (BMI), blood pressure (BP) and plasma endothelin-1 in obese hypertensive subjects. Methods . A cross sectional study was performed at National Cardiovascular Centre, Harapan Kita Jakarta, which included 80 Indonesian men. The subjects were divided into lean hypertensive and obese hypertensive. The plasma immunoreactive ET-1 and leptin were determined by ELISA method. Results . ET-1 level and leptin level were significantly higher in obese hypertensive subjects compared with lean hypertensive subjects. There are significant correlation between endothelin level with BMI (r = 0.32; p <0.005). There are also significant correlation between leptin level with BMI (r = 0.533; p <0.01), but there are no correlation between plasma leptin and endothelin-1 level in obese hypertensive men. Conclusions . Leptin and ET-1 level were significantly increase in obese hypertensive subjects compared with lean hypertensive subjects. There is no correlation between leptin and ET-1 level in obese hypertensive subjects

Effects of hypertension and obesity on the sympathetic activation of heart failure patients.

Previous studies have shown that congestive heart failure is characterized by sympathetic and reflex dysfunctions. Whether these alterations are potentiated in the presence of obesity and hypertension, two conditions that also display neuroadrenergic abnormalities and markedly increase the risk of heart failure, is unknown. In 14 healthy control subjects (C; age, 55.1+/-3.0 years; mean+/-SEM), 13 lean hypertensive subjects (H), 15 obese normotensive subjects (O), 14 lean normotensive subjects with congestive heart failure (CHF, New York Heart Association class II), 14 lean hypertensive subjects with CHF (CHFH), 14 obese normotensive subjects with CHF (CHFO), and 13 obese hypertensive subjects with CHF (CHFOH), all age-matched with C, we measured mean blood pressure (Finapres), heart rate (ECG), and muscle sympathetic nerve traffic (MSNA, microneurography) at rest and during baroreflex testing. Compared with C, body mass index was similarly increased in O, CHFO, and CHFOH, whereas mean blood pressure was similarly increased in HF, CHFH, and CHFOH, and left ventricular ejection fraction (echocardiography) was similarly reduced in CHF, CHFH, CHFO and CHFOH. Compared with C, MSNA was significantly increased in O, H, and CHF (43.0+/-2.2 versus 54.1+/-2.8, 53.1+/-2.5, and 57.4+/-2.8 bursts/100 heart beats, P<0.01). When O or H was combined with CHF, the MSNA increase was significantly more pronounced and maximal when O and H were concomitantly associated with CHF. Baroreflex sensitivity was reduced in O and H, with a further reduction in CHF and a minimal value in CHFOH. These data show that the sympathetic activation characterizing CHF is markedly potentiated when O and H alone or combined together are associated with a low cardiac output state and that this may depend on an arterial baroreflex impairment.

The relationship between body mass index and pulse pressure in older adults with isolated systolic hypertension

Background Many longitudinal studies have reported excess cardiovascular mortality among lean hypertensive subjects, suggesting that obesity may mitigate the cardiovascular risk of hypertension. Available evidence also suggests that in middle-aged and older hypertensive subjects, pulse pressure may be a better predictor of cardiovascular complications. However, there are limited data on the relationship between body mass index (BMI) and pulse pressure. Methods Using data from the Third National Health and Nutrition Examination Survey we assessed the convergence validity of pulse pressure as a predictor of cardiovascular complications and examined the relationship between BMI and pulse pressure in 1192 older adults with isolated systolic hypertension who were not receiving blood pressure medicine. Results: There was a good concordance between high pulse pressure and most of the selected cardiovascular risk factors examined in this study. Pulse pressure is higher in the lean (BMI <25) than in the overweight (BMI ≥25; 79 mm Hg vs 74 mm Hg, P < .001) and decreases significantly from 82 mm Hg in the first BMI quintile to 76 mm Hg in the fifth BMI quintile. Pulse pressure continues to decrease with increasing BMI until the index exceeds 30.1. This negative correlation persists in a multivariate model with statistical adjustment for age, sex, diabetes mellitus, and hypercholesterolemia. Conclusion The inverse relation between BMI and pulse pressure observed here may help to explain previous reports of increased cardiovascular risk among lean versus obese subjects with isolated systolic hypertension.

Antihypertensive effect of α- and β-adrenergic blockade in obese and lean hypertensive subjects

The purpose of this study was to determine the contribution of the adrenergic system in mediating hypertension in obese and lean patients. Thirteen obese, hypertensive patients with a body mass index (BMI) ≥28 kg/m 2 (obese) and nine lean patients with a BMI ≤25 kg/m 2 (lean) were recruited. After a 1-week washout period, participants underwent daytime ambulatory blood pressure monitoring (ABPM). Participants were then treated with the α-adrenergic antagonist doxazosin, titrating to 4 mg QHS in 1 week. In the next week, the β-adrenergic antagonist atenolol was added at an initial dose of 25 mg/day and titrated to 50 mg/day within 1 week. One month after the addition of atenolol, all patients underwent a second ABPM session. There were no differences between the obese and lean subjects in baseline systolic (SBP), diastolic (DBP), or mean arterial pressures (MAP) measured by office recording or ABPM. However, obese subjects had higher heart rates than lean subjects (87.5 ± 2.4 v 76.8 ± 4.9 beats/min). After 1 month of treatment with the adrenergic blockers, obese patients had a significantly lower SBP (130.0 ± 2.5 v 138.9 ± 2.1 mm Hg, P = .02) and MAP (99.6 ± 2.3 v 107.0 ± 1.5 mm Hg, P = .02) than lean patients. Obese patients also tended to have a lower DBP than lean patients (84.3 ± 2.5 v 90.9 ± 1.6 mm Hg, P = .057), but there was no significant difference in heart rate after 1 month of adrenergic blockade. These results indicate that blood pressure is more sensitive to adrenergic blockade in obese than in lean hypertensive patients and suggest that increased sympathetic activity may be an important factor in the maintenance of hypertension in obesity.

Normalization of insulin resistance in non-obese essential hypertension by cilazapril treatment.

To determine whether ACE inhibitor other than captopril improves insulin sensitivity in patients with essential hypertension, we measured insulin sensitivity to glucose utilization using SSPG method in 10 lean hypertensive subjects before and after chronic cilazapril treatment (1.5 +/- 0.2 mg/day, 15.6 +/- 2.1 weeks). The results were compared with those obtained in 10 healthy control subjects. SSPG obtained by insulin sensitivity test was significantly higher in hypertensive subjects, indicating a lower insulin sensitivity than in controls. After cilazapril treatment, SSPG reduced significantly to the level which was statistically not different from control subjects. Hyperinsulinemia diminished after treatment, while no significant change of blood glucose was observed during oral glucose tolerance test in hypertensive subjects. Plasma HDL cholesterol increased by cilazapril treatment. Cilazapril treatment has beneficial effect in the reversal of insulin resistance in patients with essential hypertension.

Higher risk of cardiovascular mortality among lean hypertensive individuals in Tecumseh, Michigan.

A cohort of 2181 men and women, aged 40 to 79 years, without evidence of coronary heart disease or cancer at entry to the Tecumseh Study was evaluated. Subjects were defined as lean if their Metropolitan Life Insurance table relative weight was < 110 (n = 584) and as obese if their relative weight was > or = 120 (n = 1024). There were 688 subjects with hypertension at study entry (systolic blood pressure > or = 160, diastolic blood pressure > or = 95, or treated). The 29-year relative risk (RR) of mortality from ischemic heart disease (IHD) or cardiovascular disease (CVD) associated with systolic blood pressure level was significant for both lean and obese subjects. Among hypertensive subjects, the RR of fatal IHD for lean versus obese hypertensive subjects was 1.87 (95% confidence interval, 1.21 to 2.88) and the RR of fatal CVD was 1.56 (95% confidence interval, 1.10 to 2.20) using a Cox proportional-hazards model to adjust for the independent effects of age and traditional CVD risk factors. The findings are consistent with other studies in men showing lean hypertensive subjects to be at greater risk of IHD or CVD mortality than obese hypertensive subjects. A similar finding is now observed in women. Associations do not prove causality or dictate management. Nevertheless, the unexplained higher mortality in lean versus obese hypertensive subjects has now been reported with sufficient frequency to suggest that the association is real (if unexplained). Determining the reasons for this association may improve targeted prevention and treatment strategies.

Endogenouw Erythropoietin Levels in patients with Obesity-Related Hypertension.

The coincidence of increased red blood cell mass with obesity and hypertension has been confirmed in a number of studies. Since erythropoietin (EPO) induces hypertonic effect, we aimed to study the possible involvement of endogenous EPO in the pathogenesis of obesity-related hypertension (ORH). Seventy-two non-obese (body mass index-BMI 30kg/m2) patients with essential hypertension, and 32 non-obese normotensive control subjects were studied on 120mmol Na/24h diets for 3 days and 30mmol Na/24h diets for the following 3 days. Serum EPO levels, plasma renin activity (PRA), aldosterone (PAC) and urinary sodium and potassium excretion were estimated under both conditions. Hematocrit, hemoglobin and serum iron, ferritin and TIBC were measured in basal conditions. Patients with ORH showed significantly higher hematocrit values, hemoglobin levels and erythrocyte counts (p<0.05) than non-obese essential hypertensives and controls, although no differences in serum EPO levels (13.6±1.1 and 12.8±1.0mU/ml, 15.3±1.2 and 13.3±1.1, 12.2±2.0 and 10.95±1.7, respectively) and log EPO×%Hct product were found between groups. In both hypertensive groups, BMI but not blood pressure positively correlated with hematocrit. A negative correlation between changes in EPO and PRA induced by sodium restriction was found in lean hypertensive subjects only (r =-0.42, p<0.01). This finding suggests that in contrast to non-obese patients with essential hypertension, in subjects with ORH activity of the renin-angiotensin-aldosterone system does not seem to be related to EPO secretion. Since in both lean and obese essential hypertensive subjects EPO and log EPO ×%Hct product are within normal range, the contribution of endogenous EPO to the pathogenesis of hypertension in these patients is unlikely. (Hypertens Res 1994; 17: 43-48)

Risk factors for subarachnoid hemorrhage in a longitudinal population study

The known risk factors of atherosclerotic diseases may be involved in the development of a subarachnoid hemorrhage. We studied the morbidity and mortality due to subarachnoid hemorrhage among 42,862 men and women aged 20–69 years who had participated in a large health survey in Finland. During a mean follow-up of 12 years, 102 non-fatal and 85 fatal cases of subarachnoid hemorrhage were observed. The total incidence was 37 per 100,000 person-years. Smoking and hypertension were positively associated and body mass index was inversely associated with the risk of subarachnoid hemorrhage. These associations were not confounded by age or each other. No statistically significant association with risk was detected for serum cholesterol level, hematocrit content, known heart disease, or diabetes. The risk was especially elevated among lean hypertensive subjects and lean smoking subjects. The age-adjusted relative risks of subarachnoid hemorrhage for lean, hypertensive smokers were 18.3 (95% confidence interval (CI), 7.8–42.7) among women and 6.7 (95%Cl, 2.3–19.7) among men as compared to the risk among subjects without these risk factors. We conclude that modifiable risk factors are predictive of subarachnoid hemorrhage, for which reason subarachnoid hemorrhage may in part be preventable. Leanness combined with arterial hypertension and/or smoking, in particular, poses a substantially elevated risk.

LEUCOCYTE SODIUM CONTENT AND SODIUM PUMP ACTIVITY IN OVERWEIGHT AND LEAN HYPERTENSIVES

Leucocyte sodium content and sodium pump activity was studied in overweight and lean hypertensive subjects and normotensive controls, all in the fasting state. In lean subjects (body mass index less than 27 kg m-2), hypertensives did not have altered leucocyte sodium content or pump activity. In the overweight (mostly obese) subjects, the leucocyte sodium content was higher in hypertensive than in normotensive subjects (median (range) 56.1 (42.0-84.1) vs 32.0 (18.2-59.4) mmol kg-1, P less than 0.001). This raised sodium content in overweight hypertensives was associated with a lower (ouabain-sensitive) 22Na efflux rate constant (2.25 (1.15-3.01) vs 2.64 (1.98-3.61) h-1, P less than 0.05) and a higher passive (or ouabain-insensitive) 22Na efflux rate constant (0.90(0.53-1.18) vs 0.63 (0.21-1.09) h-1, P less than 0.01). The systolic and diastolic blood pressures were significantly correlated to intracellular Na+ in the overweight group (r = 0.41 and 0.56, P less than 0.02 and 0.001 respectively). Thus, hypertension in the overweight subjects is associated with accumulation of intracellular sodium that may be due to abnormalities of the active sodium pump, though changes in ouabain-insensitive mechanisms also occur.