NORMAL BLOOD PRESSURE IN OBESITY IS ASSOCIATED WITH REDUCED PERIPHERAL VASCULAR RESISTANCE: 8B.05

Abstract

Objective: The link between obesity and elevated blood pressure is firmly established. However, not all obese individuals are hypertensive, suggesting that adaptive mechanisms are present in at least some obese individuals which allow them to maintain normal levels of blood pressure (BP). The aim of the current study was to examine the mechanisms underlying different levels of BP in obese individuals. Design and Method: Data from 2511 individuals (1262 males) were available from The Enigma Study for the current analyses. All individuals were aged between 18–40 years, and were free of cardiovascular disease and medication. Detailed demographic, biochemical and haemodynamic data, including BP, cardiac output (CO) and peripheral resistance (PVR) were obtained in all individuals. They were then stratified according to BMI (normal weight, overweight and obese) using WHO criteria, and seated brachial BP (optimal, normal, high-normal and hypertensive) using JNC 6 criteria. For the current analyses, comparisons were made between 3 groups: normal-weight normotensives (controls, optimal and normal BP, n = 1360), obese normotensives (optimal and normal BP, n = 61) and obese hypertensives (n = 79). Results: Compared with controls, obese individuals were older, had an increased family history of hypertension and an adverse biochemical profile (P < 0.01 for all). In addition, heart rate, CO and stroke volume were all significantly elevated in obese individuals (P < 0.001 for all). However, the elevation in CO was more marked in obese individuals who were hypertensive (P < 0.05 versus obese normotensives). In contrast, PVR was significantly lower in obese individuals with normal BP (P < 0.05 versus controls and obese hypertensives). Conclusions: These data suggest that a reduction in peripheral resistance is an important mechanism by which some obese individuals maintain normal blood pressure despite having a significantly elevated cardiac output. Although the factors underlying the reduction in PVR in these individuals remain to be elucidated, they are likely to provide an intriguing insight into the pathophysiology of obesity-related hypertension.