Brachial artery vasomotor function is inversely associated with 24-h ambulatory blood pressure.

BACKGROUND

Impaired endothelial function has been reported in hypertensive individuals. The extent to which such changes reflect the co-existence of other cardiovascular disease risk factors rather than an independent association with blood pressure remains uncertain.

OBJECTIVE

To assess the relationship between brachial artery vasomotor function and ambulatory blood pressure in hypertensive individuals and normotensive controls.

METHODS

We assessed 24-h ambulatory blood pressure and brachial artery endothelial and smooth muscle function in 155 patients with hypertension and 40 normotensive controls. The vasomotor functions were determined by ultrasonographic assessment of vasodilator responses to flow and sublingual glyceryl trinitrate, respectively. Patients with hypertension were categorized as either treated (n = 85) or untreated (n = 70), and further subdivided on the basis of either no or at least one other cardiovascular risk factor. These included hyperlipidaemia, smoking, diabetes or a previous coronary or cerebrovascular event.

RESULTS

Age- and sex-adjusted flow-mediated and glyceryl trinitrate-mediated responses were not significantly different in hypertensive individuals with respect to treatment status or the presence of risk factors when compared with controls. However, when data from all 195 study participants were pooled, 24-h ambulatory systolic blood pressure was inversely related to flow-mediated response (P = 0.002), and both systolic and diastolic blood pressure were inversely related to glyceryl trinitrate response (P < 0.001 and P = 0.009, respectively). Observed relationships were largely unaltered after further adjustment for body mass index, antihypertensive treatment or the presence of other risk factors.

CONCLUSIONS

The finding of a direct and inverse relationship between the level of ambulatory blood pressure and flow-mediated and glyceryl trinitrate responses is consistent with a direct influence of blood pressure on conduit vessel vascular function.