The hemodynamic response to emotional stress (mental arithmetic) was studied in ten borderline and ten mild hypertensives in comparison to ten age-matched normotensives. Due to emotional stress the blood pressure increased in all three groups; its rise was greater in borderline and mild hypertension. After stress, the blood pressure also remained elevated longer in the hypertensive groups. The increased blood pressure reaction was accompanied by a greater rise of heart rate and cardiac output. The increase of cardiac output correlated with the blood pressure elevation. Stroke volume changed in comparison to the pre-stress period only in the mild hypertension group. Total peripheral resistance decreased slightly in all three groups. No significant differences between the groups could be found in regard to stroke volume and total peripheral resistance. The cardiovascular hyperreactivity in early hypertension is attributed to a stronger sympathetic stimulation of the circulation. The hemodynamic pattern indicates an increased beta-adrenergic stimulation of the heart as the main pathological mechanism.

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The influence of beta blockers on Type A behavior pattern and cardiovascular reactivity was tested. Nineteen white, male hypertensive patients were divided at random into two therapeutic groups (100 mg atenolol versus 50 mg hydrochlorothiazide + 5 mg amiloride (control group) ). For each patient, the German version of the structured interview was performed before therapy and at a minimum of 4 weeks after normalization of clinical resting casual blood pressure (BP). Prior to therapy, there were no differences in age, BP at rest, cardiovascular reactivity, and Type A between the two groups. After therapy, the patients treated with beta blockers changed Type A characteristics toward Type B, regardless where they started on the Type A scale, and beta blockers attenuated cardiovascular reactivity. In this study, Type A (hypertensive patients) was not associated with greater cardiovascular reactivity.

All available polycyclic aromatic hydrocarbon ( PAH ) concentration data in ambient air obtained over the past 10 years in Germany were evaluated to clarify whether it is justified to use benzo( a )pyrene ( BaP ) as a marker compound for the total PAH exposure. The data basis comprises annual mean concentrations from 1990 to 1998 supplied by the emission protection authorities of the federal states with additional information on the region, year and site of measurement. The data are very heterogeneous with respect to sample size, the number of individual PAHs analyzed, place of origin and year. Nine of 25 individual compounds with sufficient sample size ( 74 < N < 518 ) were submitted to an explorative descriptive analysis and multiple regression analysis. Six compounds were selected for factor analysis to evaluate whether associations can be related to one or several background determinants. The concentration data of BaA, BeP, BaP, DBA, BghiP, COR, BbF, BkF and INP are not normally distributed and demonstrate great variability. Location, East -West differences persisting after the German reunion and time characterize the distributive patterns, e.g., from 1991 to 1997, a significant decrease in BaP could be determined based on the data from North Rhine -Westphalia ( 1991, N = 51, median 1.6 ng / m 3 ; 1997, N = 45, median 0.7 ng / m 3 ; P 0.0001 ). The BaP concentrations in the new federal states in the East ( N = 80, median 2.2 ng / m 3 ) are about twice as high compared to the ones in the old federal states in the West ( N = 438, median 1.1 ng / m 3 ; P 0.0001 ). BaP measurements taken at sites characterized by traffic ( 1.8 ng / m 3 ), industrial ( 1.3 ng / m 3 ) or urban environment ( 1.3 ng / m 3 ) rank significantly higher compared to measurements taken at rural sites ( 0.92 ng / m 3 ; P 0.0001 ). Factor analysis of the intercorrelation matrix of BaA, BeP, BaP, DBA, BghiP and COR yields one factor to explain 92% of the variability of the six individual PAHs. BaP shows the highest factor loading. These results confirm the common practice to use BaP as marker compound for the PAH exposure in ambient air.