Differential glucose tolerance in dipper and nondipper essential hypertension: the implications of circadian blood pressure regulation on glucose tolerance in hypertension.
OBJECTIVE
The goals of this study were to compare glucose tolerance in dipper and nondipper hypertensive patients and to explore the cause of glucose intolerance in essential hypertension.


METHODS
A total of 50 patients <45 years old who had essential hypertension were recruited and studied by 24-h blood pressure monitoring and an oral glucose tolerance test (OGTT). Autonomic function was assessed with spectral analysis of heart rate variability


RESULTS
Dipper hypertensive patients (n=25) had lower nocturnal blood pressure than nondipper (n=25) patients. During OGTT, postprandial glucose levels were higher in the nondippers at 0, 90, and 120 min (all P < 0.05). Nondippers had a higher fasting insulin/glucose ratio than was apparent in normal control subjects. Despite higher postprandial glucose levels, nondippers had lower postprandial insulin levels. These results suggest that nondippers were insulin resistant and that their pancreatic beta-cell function was impaired. For all patients, nocturnal reduction of blood pressure was inversely related to total glucose levels under the OGTT curve and was positively related to postprandial insulin levels. Daytime heart rate did not differ between the dippers and nondippers, but nocturnal heart rate was higher in the nondippers, suggesting that nocturnal sympathetic activities were higher among the nondippers. Spectral analysis of heart rate variability suggests that the nondippers had lower parasympathetic activities and unbalanced sympathetic/parasympathetic outflow.


CONCLUSIONS
These findings indicate that nondipper hypertensive patients are more glucose intolerant than are dipper patients. The abnormalities of glucose metabolism in nondippers could be explained by insulin resistance and beta-cell dysfunction. The results of spectral analysis suggest that abnormal autonomic outflow may represent a possible link between hypertension and associated metabolic dysfunction.
Chen
J W
JW
Department of Medicine, Veterans General Hospital, Taipei, Taiwan.
Jen
S L
SL
Lee
W L
WL
Hsu
N W
NW
Lin
S J
SJ
Ting
C T
CT
Chang
M S
MS
Wang
P H
PH
D000328:Adult; D000450:Aldosterone / Q000097:blood; D001341:Autonomic Nervous System / Q000503:physiopathology; D001786:Blood Glucose / Q000378:metabolism*; D001794:Blood Pressure / Q000502:physiology*; D002395:Catecholamines / Q000652:urine; D002784:Cholesterol / Q000097:blood; D002940:Circadian Rhythm / Q000502:physiology*; D003971:Diastole; D004837:Epinephrine / Q000097:blood; D005260:Female; D005951:Glucose Tolerance Test; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000097:blood* / Q000503:physiopathology* / Q000652:urine; D008297:Male; D009638:Norepinephrine / Q000097:blood; D019518:Postprandial Period; D013599:Systole; D014280:Triglycerides / Q000097:blood
D001786:Blood Glucose; D002395:Catecholamines; D014280:Triglycerides; D000450:Aldosterone; D002784:Cholesterol; D009638:Norepinephrine; D004837:Epinephrine