We tested the reproducibility of ambulatory blood pressure monitoring (ABPM) by the use of agreement plots. Thirty-two normotensive volunteers underwent ABPM on four separate days (interval 28 days), on the same typical weekday. Sleeping time was restricted to the ABPM nighttime subperiod from 11:00 PM to 7:00 AM. Twenty-four-hour average values-both systolic and diastolic-daytime average values, and nighttime average values, as well as standard deviation (SD) values, were analyzed for differences (analysis of variance). Adaptation occurred from the first to the fourth ABPM, ie, average 24 h, daytime, and nighttime values were lower (-1 to -3 mm Hg) during the fourth recording than the first (P < .05 to P < .01). The agreement analysis showed a surprisingly high agreement among the four data sets (ie, differences from +/-2.54 to +/-5.92 mm Hg; +/-2 SD of the distribution). We concluded that reproducibility of ABPM seems excellent, but adaptation may occur, even in normotensive volunteers under research conditions. Caution must be paid before labeling a patient as hypertensive, because initial ABPM may yield higher values than later monitorings.
We present a method involving minor modifications of previous techniques, in which we use an ion-pair reversed-phase HPLC separation with three-electrode coulometry. Isocratic baseline separations can be obtained in 5 min. The sample preparation procedure, involving extraction with alumina at low temperature, allows good reproducibility (within-run and between-run CVs less than 10%) and improved sensitivity (less than 5 pg of each catecholamine per extract). This method allows approximately 70 low-cost plasma catecholamine analyses to be done in a working day.
The purpose of this study has been to test the hypothesis of an alpha 2-adrenoreceptor alteration in human essential hypertension. The design of the study involved the oral administration of 10 mg yohimbine, an alpha 2-adrenergic antagonist, to 25 healthy volunteers and 29 sex- and age-matched untreated hypertensive patients. Volunteers and patients were studied twice in random order, after placebo or yohimbine treatment, in supine and upright positions. Arterial pressure and heart rate were monitored by servoplethysmomanometry, and venous plasma catecholamines were determined by HPLC with electrochemical detection. Yohimbine induced a significant increase in diastolic pressure only in the hypertensive patients. Plasma norepinephrine was increased significantly in both yohimbine-treated groups, but the percent increase of plasma norepinephrine after the standing test was decreased significantly only in the healthy yohimbine-treated subjects. Plasma dopamine was increased significantly only in the healthy yohimbine-treated subjects. The response of plasma dopamine to the upright position was modified only in the healthy yohimbine-treated subjects. The decrease observed after 2 min of standing was abolished, showing the involvement of alpha 2-adrenoreceptors in the physiologic response of plasma catecholamines in healthy volunteers. Our data may be consistent with some in vivo evidence of an alpha 2-adrenoreceptor desensitization or an alteration in the balance of alpha-adrenoreceptors in human hypertension.
In 9 normotensive uremic patients undergoing chronic hemodialysis, the baseline plasma catecholamines varied widely from low-normal to very high; sulfoconjugated plasma catecholamines were constantly high. A dialysis-induced fall of all sulfated catecholamines and epinephrine was observed. Norepinephrine decreased in 5 patients and increased in 4, with a strong inverse correlation between predialysis norepinephrine and Δ norepinephrine (p < 0.0001). No correlation was evident between clinical parameters (mean arterial pressure, heart rate) and catecholamines (both predialysis and postdialysis). Significant (p < 0.0001 and p < 0.0002) inverse correlations between epinephrine and norepinephrine and their sulfoconjugation degree were demonstrated only in predialysis. Our data may support the presence of a uremic autonomic neuropathy and adrenoceptor damage.
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