Our laboratory investigated the earliest phases of hypertension in order to separate primary from secondary (pressure-induced) phenomena. Repeatedly, we found abnormalities of the autonomic control of hemodynamics combined with characteristic personality traits in patients with borderline hypertension. Due to invasive methodology, progress was slow and it took us 18 years to complete measurements in 220 BH and 190 control subjects. The possible preselection of volunteers for invasive studies could have affected the general applicability of our results. Furthermore, not all borderlines will develop established hypertension, and it is not known which of the abnormalities found in the laboratory are relevant to future hypertension. Recently the situation has changed. a) New, reliable noninvasive hemodynamic methods were cross-validated in our laboratory. b) We have new methods for assessing target organ damage and the patients' average BP levels. This permits stratifying BH by """"""""severity"""""""" and thus by degree of likelihood to develop """"""""true"""""""" hypertension. c) Tests to evaluate sympathetic function are simplified and applicable to large studies. d) Therefore, it is now possible to mount a field study in the village of Tecumseh, Michigan, where extensive records on BP in families are available. The goal is to organize a population-based study of physiologic and behavioral precursors of hypertension. We wish to know a) the prevalence of the hyperadrengergic state among unselected subjects with borderline hypertension, b) are personality traits (submissiveness, anger) found in the laboratory also descriptive of and specific for free-living patients with borderline hypertension, c) are the hyperadrenergic state and a specific personality pattern associated, and how do they relate to risk of hypertension? The second aim of this proposal is to select subjects with highest risk for hypertension and study them in detail. They will be reexamined after three years in order to learn about the stability of psychophysiologic interactions in borderline hypertension, and to draw inferences about pathophysiology of hypertension.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Method to Extend Research in Time (MERIT) Award (R37)
Project #
5R37HL037464-04
Application #
3486162
Study Section
Behavioral Medicine Study Section (BEM)
Project Start
1987-02-01
Project End
1992-01-31
Budget Start
1990-03-01
Budget End
1991-01-31
Support Year
4
Fiscal Year
1990
Total Cost
Indirect Cost
Name
University of Michigan Ann Arbor
Department
Type
Schools of Medicine
DUNS #
791277940
City
Ann Arbor
State
MI
Country
United States
Zip Code
48109
Julius, S; Nesbitt, S (1998) Clinical consequences of the autonomic imbalance in hypertension and congestive heart failure. Scand Cardiovasc J Suppl 47:23-30
Julius, S (1998) Effect of sympathetic overactivity on cardiovascular prognosis in hypertension. Eur Heart J 19 Suppl F:F14-8
Julius, S; Palatini, P; Nesbitt, S D (1998) Tachycardia: an important determinant of coronary risk in hypertension. J Hypertens Suppl 16:S9-15
Nesbitt, S D; Amerena, J V; Grant, E et al. (1997) Home blood pressure as a predictor of future blood pressure stability in borderline hypertension. The Tecumseh Study. Am J Hypertens 10:1270-80
Amerena, J; Nesbitt, S; Krause, L et al. (1997) Trends in left ventricular function over three years in the Tecumseh Study. Blood Press 6:262-8
Vriz, O; Nesbitt, S; Krause, L et al. (1997) Smoking is associated with higher cardiovascular risk in young women than in men: the Tecumseh Blood Pressure Study. J Hypertens 15:127-34
Palatini, P; Julius, S (1997) Heart rate and the cardiovascular risk. J Hypertens 15:3-17
Julius, S; Nesbitt, S (1996) Sympathetic overactivity in hypertension. A moving target. Am J Hypertens 9:113S-120S
Kjeldsen, S E; Moan, A; Petrin, J et al. (1996) Effects of increased arterial epinephrine on insulin, glucose and phosphate. Blood Press 5:27-31
Julius, S; Nesbitt, S D (1996) Sympathetic nervous system as a coronary risk factor in hypertension. Cardiologia 41:309-17

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