FAMILIAL HYPERTENSION, INSULIN, SYMPATHETIC ACTIVITY, AND BLOOD-PRESSURE ELEVATION

Citation
K. Masuo et al., FAMILIAL HYPERTENSION, INSULIN, SYMPATHETIC ACTIVITY, AND BLOOD-PRESSURE ELEVATION, Hypertension, 32(1), 1998, pp. 96-100
Citations number
30
Categorie Soggetti
Peripheal Vascular Diseas
Journal title
ISSN journal
0194911X
Volume
32
Issue
1
Year of publication
1998
Pages
96 - 100
Database
ISI
SICI code
0194-911X(1998)32:1<96:FHISAA>2.0.ZU;2-Q
Abstract
This study evaluated the effects of a positive family history of hyper tension (FH+) on the contributions of sympathetic nervous system (SNS) activity and insulin to blood pressure elevation (BPE). The study des ign was longitudinal and evaluated BP, body mass index (BMI), and fast ing plasma insulin and norepinephrine (NE) levels for 10 years in 557 young, nonobese Japanese men who were normotensive at entry. FH+ was d efined as hypertension in first-degree relatives as verified by histor ical records or direct determination. BPE was defined as a greater tha n or equal to 10% rise in systolic and diastolic BP over entry levels during the 10-year period. In the total group FH+ was noted in 16%, an d BPE occurred in 18% of normotensive subjects. When evaluated by FH, the prevalence of BPE was 33% in FH+ compared with 16% in FH- (P<0.05) . BP levels were greater both at entry and at year 10 in the FH+ group . The absolute increment in plasma NE over 10 years was greater in the BPE group than in those without BPE (P<0.01). Of note, the rise in pl asma NE levels in BPE individuals was identical in FH+ and FH- subject s. Plasma insulin increments were also greater in normotensive subject s with BPE than in normotensive subjects without BPE. However, compare d with NE, development of hyperinsulinemia was mon pronounced in the F H+ subjects. The results indicate that SNS hyperactivity may be a less genetically determined predictor of hypertension than is hyperinsulin emia. Because SNS changes in this initially normotensive population ap peared more closely related to the development of hypertension than to hyperinsulinemia, environmental rather than genetic factors may be th e main determinant of early BPE in nonobese normotensive subjects.