Does sympathoadrenal activity predict changes in body fat? An 18-y follow-up study.

BACKGROUND: Whether alterations in the sympathoadrenal system contribute to obesity or, rather, are consequences of it, is an unresolved issue. OBJECTIVE: We hypothesized that the sympathoadrenal system plays a predictive role in the development of body fat. DESIGN: At entry, arterial plasma epinephrine and norepinephrine concentrations were measured in 99 healthy men (x +/- SD age: 19.3 +/- 0.4 y) at rest and during a mental stress test and a cold pressor test. Body mass index (BMI; in kg/m(2)), waist circumference, and triceps skinfold thickness were measured at entry and after 18 y of follow-up. RESULTS: Eighty subjects (81%) were available for follow-up analyses after a mean (+/-SD) of 18.0 +/- 0.9 y. The epinephrine responses to the mental stress test (E(MST)) showed a negative relation to changes in BMI (P = 0.01) and waist circumference (P = 0.007). The mean increase in BMI was 6.3 among subjects in the lowest E(MST) quartile and 3.7 in the remaining subjects. In multiple regression analyses corrected for level of exercise, BMI, waist circumference, and triceps skinfold thickness at entry, E(MST) was found to be a consistent negative predictor of future BMI (P = 0.005), waist circumference (P = 0.001), and triceps skinfold thickness (P = 0.05). CONCLUSIONS: We present the first long-term follow-up study in whites showing that the epinephrine response to mental stress is a negative predictor of future BMI, waist circumference, and triceps skinfold thickness after 18 y of follow-up. These findings may provide further insights into the pathophysiology of obesity.

Sympathoadrenal stress reactivity is a predictor of future blood pressure: an 18-year follow-up study.

In the present study we hypothesized that arterial catecholamine concentrations during rest and 2 laboratory stress tests were independent predictors of blood pressure at an 18-year follow-up. At entry, blood pressure, heart rate, and arterial plasma epinephrine and norepinephrine concentrations were measured in 99 healthy men (age: 19.3+/-0.4 years, mean+/-SD) at rest, during a mental arithmetic test, and during a cold pressor test. After 18.0+/-0.9 years of follow-up, resting blood pressure was measured. The norepinephrine and epinephrine concentrations during the mental arithmetic explained 12.7% of the variation of future systolic blood pressure after adjusting for initial resting blood pressure, family history, body mass index, and systolic blood pressure during the stress test in a multiple regression analysis (adjusted R(2)=0.651; P<0.001). To conclude, the present study shows that sympathetic nervous activity during mental arithmetic predicts future blood pressure, indicating a possible causal factor in the development of essential hypertension independent of the initial blood pressure.

Do screening blood pressure and plasma catecholamines predict development of hypertension? Twenty-year follow-up of middle-aged men.

OBJECTIVES: The sympathetic nervous system is implicated in the development and maintenance of hypertension. However, the predictive impact of arterial plasma catecholamines has never been reported. We investigated arterial catecholamines and blood pressures (BPs) prospectively over 20 years in a group of well-characterized middle-aged men. METHODS: Fifty-six of original 79 men were available for the follow-up. Multiple regression analysis was done with mean BP at follow-up as a dependent variable, and arterial plasma catecholamines and BP at baseline as independent variables. RESULTS: Half of the originally normotensive men developed hypertension during follow-up. There were significant differences in the screening BP values measured at baseline between the new hypertensives and the sustained normotensives. Multiple regression analysis revealed arterial adrenaline at baseline as an independent predictor of mean BP at follow-up in the new hypertensives (beta = 0.646, R2 = 0.42, p = 0.007). Furthermore, arterial noradrenaline at baseline was a negative independent predictor of mean BP at follow-up in the sustained normotensives (beta = -0.578, R2 = 0.334, p = 0.020). Noradrenaline increased with age in the group as a whole (1318+/-373 vs 1534+/-505 pmol/l, p = 0.010) while adrenaline did not change. CONCLUSION: Our data suggest that arterial adrenaline is involved in the development of hypertension over 20 years in middle-aged men. Men with sustained normotension may have an inherent protection against sympathetic overactivity. Furthermore, screening BP at baseline in normotensive men differentiated between those who developed hypertension and those who remained normotensive at follow-up.

Adrenaline during mental stress in relation to fitness, metabolic risk factors and cardiovascular responses in young men.

We studied plasma adrenaline (A) in relation to physical fitness, metabolic cardiovascular risk factors and cardiovascular responses. Men (age 21-24 years) with high and normal (both n=19) screening blood pressure (BP) were studied cross-sectionally. We measured peak oxygen uptake (VO2peak) (treadmill exercise), and plasma catecholamines, heart rate (HR), finger systolic (SBP) and diastolic (DBP) BP, and insulin-adjusted glucose disposal rate (GDR/I) during a hyperinsulinaemic glucose clamp (rest) and mental arithmetic stress test (MST). By multiple regression, A at rest (Arest) (beta=0.37, p<0.05) and during MST (Amst) (beta=0.40, p<0.01) were associated with high screening BP. In the respective models, Arest was negatively related to body mass index (BMI) (beta=-0.56, p<0.001) and Amst positively to VO2peak (beta=0.54, p<0.001). BP and HR responses correlated positively with VO2peak, but were determined by Amst in multiple regression models. Independently of BMI and VO2peak, serum high-density lipoprotein cholesterol was positively related to A levels, whereas GDR/I was independently related only to VO2peak. Increased adrenaline secretion may be related to high BP, but may at the same time be associated with a beneficial metabolic profile.

Low-renin status in therapy-resistant hypertension: a clue to efficient treatment.

OBJECTIVE: Therapy resistance is an enduring problem in clinical hypertension. Our aims were to estimate: (1) the contribution of a low-renin status in therapy resistance; (2) whether such status could give a clue to more successful treatment; and (3) the contribution by adrenal cortical adenomas and by primary aldosteronism. SETTING: Patients were referred from general and internal medicine practices following written invitations and included consecutively. Participants were examined and followed-up on an outpatient basis. DESIGN AND INTERVENTIONS: Patients were divided according to renin status. Low-renin patients were treated with an aldosterone inhibitor in a prospective, randomized, placebo-controlled, double-blind, cross-over study. MAIN OUTCOME MEASURES: Prevalence of low-renin status in therapy resistance. Blood pressure and hormonal responses to specific treatment. Numbers of adrenocortical adenomas and primary aldosteronism. RESULTS: In 90 treatment-resistant hypertensive, 67% had plasma renin activity (PRA) below 0.5 nmol/l per hour. Of the 60 low-renin patients, 38 were studied on a fixed combination of amiloride and hydrochlorothiazide. Three weeks' treatment reduced blood pressure by 31/15 mmHg compared to placebo (P < or = 0.0001). Serum aldosterone and plasma renin activity increased substantially during active treatment. Through the subsequent 6-12 months of open treatment, seven patients (18%) showing an escape phenomenon had their high blood pressure effectively treated by extra amiloride. Of the 60 low-renin patients, eight had adrenal adenoma. CONCLUSION: A low-renin status characterized two-thirds of patients with treatment-resistant hypertension, who could be treated efficiently by aldosterone inhibition. Patients with an escape phenomenon (18%) could effectively be treated by increasing the aldosterone inhibitor. Low-renin hypertensives had high prevalence of adrenocortical adenomas and primary aldosteronism.