| Summary: | Flow mediated dilatation (FMD) is an accepted, non-invasive measure of endothelial function. FMD measures the capacity of the endothelium to respond to a stimulus but does not assess resting vascular tone. Prior to the measurement of FMD, the radial artery constricts as blood flow to the hand is interrupted, a phenomenon termed low-flow mediated constriction (FMC). The mechanisms of FMC remain poorly understood, however this measure is complementary to FMD. For example, exercise leads to vascular stimulation with an acute reduction in FMD but a reciprocal increase in FMC. It was hypothesized that interventions, which modify vascular nitric oxide bioavailability and alter endothelial function, impact FMC in normal subjects. The first protocol examined the impact of continuous therapy with transdermal nitroglycerin (GTN) on FMD and FMC (n = 18). After 5-7 days of GTN therapy, radial artery size was larger than before GTN (P < 0.01), FMD was reduced (P < 0.02, fig) but FMC was unchanged. In the second protocol (n = 8), vascular responses were assessed during sustained GTN therapy and 2 hours after GTN removal. FMD was blunted in the presence of GTN and remained blunted 2 hours after GTN removal (P < 0.01, fig), when vessel diameter had returned to baseline, but FMC was unchanged. In a third protocol (n = 14), the effect of inhaled salbutamol on vascular function was examined. Following stimulation with salbutamol, FMD was depressed (P < 0.02, fig) but FMC was not changed. These observations demonstrate that FMC does not change in response to sustained therapy with GTN, an intervention associated with marked abnormalities in endothelium dependent vasomotor responses, nor in response to beta-2 adrenergic receptor stimulation, an intervention known to acutely modify endothelial function. Both interventions are felt to mediate their effects through modification of nitric oxide bioavailability. Therefore, these findings confirm that FMC is not primarily dependent on nitric oxide.
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