Weight gain-induced blood pressure elevation

This study was conducted to evaluate the mechanisms in weight gain-induced blood pressure (BP) elevation focusing, in particular, on the contributions of sympathetic nervous system activity, fasting plasma insulin, and leptin to BP levels. The study design was longitudinal with a cohort of 1897 men. BP, pulse rate, body mass index (BMI), fasting plasma norepinephrine (NE), insulin, and leptin were measured at 6 and 12 months in those 172 lean nor motensive, 79 obese normotensive, 64 lean untreated hypertensive, and 38 ob ese untreated hypertensive men whose BMI increased >10% during the first 6 months. At entry, levels of BP, pulse rate, plasma NE, insulin, and leptin in obese subjects, regardless of BP status, were significantly greater than those in lean subjects. The levels of plasma NE, insulin, and leptin incre ased with weight gain in the 4 study groups. In the subjects with BP elevat ion, the increase in pulse rate and plasma NE was significantly greater tha n that in the subjects without BP elevation at both 6 and 12 months for eac h of the 4 study groups, although the increase in BMI was similar between t he subjects with and without BP elevation. In obese but not lean subjects, whether normotensive or hypertensive, the increases in plasma insulin and p lasma leptin with weight gain were greater in the subjects with accompanyin g BP elevation compared with the subjects without BP elevation. On the othe r hand, at 6 months in lean subjects, the increase in plasma insulin with w eight gain in the subjects with BP elevation was actually lower than that i n the subjects without BP elevation. These results suggest that weight gain -induced sympathetic overactivity is more tightly linked to weight gain-ind uced BP elevation than the changes in plasma insulin and leptin that also a ccompany weight gain. It is probable that sympathetic nervous activation wi th weight gain is a major mechanism of blood pressure elevation. Hyperinsul inemia and hyperleptinemia may be ancillary factors that contribute to symp athetic nervous stimulation with weight gain.