Effect of propranolol on sympathetically mediated leg vasoconstriction in humans

Sympatho-excitatory manoeuvres are used to study vascular responsiveness in humans, but it is unclear if circulating adrenaline attenuates peripheral vasoconstriction during these manoeuvres. We hypothesized that vasoconstrictor responses to three manoeuvres (neck pressure, unilateral thigh-cuff release and isometric handgrip) would be greater after the administration of the β-adrenergic blocker propranolol. Seven men and six women underwent these manoeuvres while beat-by-beat arterial pressure (finger photoplethysmography), femoral mean blood velocity (Doppler ultrasound) and femoral artery diameter (edge-detection software) were measured. Femoral vascular conductance was calculated as flow/pressure. Propranolol had no effect on baseline femoral vascular conductance ( P > 0.05). As a result of neck pressure, femoral vascular conductance was reduced 23.9 ± 3.5% before vs . 33.2 ± 3.2% after infusion of propranolol ( P = 0.033). After thigh-cuff release, femoral vascular conductance declined 50.2 ± 5.8% before vs . 57.4 ± 9.6% after propranolol infusion ( P = 0.496). During handgrip, femoral vascular conductance was reduced 47.2 ± 9.6% before vs . 55.2 ± 9.2% after propranolol administration ( P = 0.447). After handgrip, women had a greater rise in conductance than men (women: 153 ± 16.2%; men: 36.4 ± 10.6%; P < 0.001), which was blunted by 54.8% by propranolol ( P < 0.001 vs . control), but unaffected by propranolol in men ( P = 0.355 vs . control). The finding that β-adrenergic receptor-mediated vasodilatation minimally affects vascular responses to these sympatho-excitatory manoeuvres reinforces their utility in the investigation of sympathetic vascular regulation in humans. Interestingly, post-handgrip hyperaemia is greater in women than men and is, in part, β-adrenergic receptor mediated.