title: Differences in insulin and sympathetic responses to glucose ingestion due to family history of hypertension.
abstract: To evaluate the relationship of metabolic and neural factors in familial hypertension, we examined blood pressure (BP), blood glucose, and plasma insulin and norepinephrine (NE) levels before and every 30 min for 120 min after glucose ingestion in six groups with 20 subjects each: normotensive subjects (NT) with and without a family history of hypertension; borderline hypertensive patients (BHT) with and without a family history of hypertension; and established hypertensive patients (EH) with and without a family history of hypertension. The changes in blood glucose were similar in the six groups. In the subjects with a positive family history of hypertension regardless of BP levels, the basal levels and changes in insulin levels after glucose ingestion were significantly greater than those in the subjects without a family history of hypertension (F = 13.32, P = .0001). In BHT and EH subjects, regardless of family history, changes in insulin were greater than in NT (F = 16.00, P = .0001). Basal levels and changes in plasma NE were higher in BHT and EH (F = 26.55, P = .0001) than NT and changes in plasma NE were greater in subjects with a family history than those in subjects without a family history (F = 18.32, P = .0001). Thus, abnormal insulin and NE responses to glucose appear to aggregate in subjects with a history of familial hypertension, regardless of the level of BP. Furthermore, the ratio of delta NE/ delta insulin (changes from basal to peak) in NT and BHT, and in subjects with a family history were significantly greater than in EH and in subjects without a family history. Thus, we demonstrated that concomitant abnormalities in the glucose-insulin regulatory system and the sympathetic nervous system characterize the early phase in the development of hypertension and these abnormalities have an apparent genetic basis.
authors.affiliation: Department of Geriatric Medicine, Osaka University Medical School, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Masuo
authors.forename: H
authors.initials: H
authors.lastname: Mikami
authors.forename: T
authors.initials: T
authors.lastname: Ogihara
authors.forename: M L
authors.initials: ML
authors.lastname: Tuck
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002784:Cholesterol / Q000097:blood; D005947:Glucose / Q000008:administration & dosage / Q000494:pharmacology*; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000235:genetics* / Q000503:physiopathology*; D007328:Insulin / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009638:Norepinephrine / Q000097:blood; D013564:Sympathetic Nervous System / Q000187:drug effects*
chemical_list: D001786:Blood Glucose; D007328:Insulin; D002784:Cholesterol; D005947:Glucose; D009638:Norepinephrine