α-Adrenergic vasoconstrictor responsiveness is preserved in the heated human leg.

This study tested the hypothesis that passive leg heating attenuates α-adrenergic vasoconstriction within that limb. Femoral blood flow (FBF, femoral artery ultrasound Doppler) and femoral vascular conductance (FVC, FBF/mean arterial blood pressure), as well as calf muscle blood flow (CalfBF, ¹³³xenon) and calf vascular conductance (CalfVC) were measured during intra-arterial infusion of an α₁-adrenoreceptor agonist, phenylephrine (PE, 0.025 to 0.8 μg kg₋₁ min₋₁) and an α₂-adrenoreceptor agonist, BHT-933 (1.0 to 10 μg kg₋₁ min₋₁) during normothermia and passive leg heating (water-perfused pant leg). Passive leg heating (∼46◦C water temperature) increased FVC from 4.5 ± 0.5 to 11.9 ± 1.3 ml min₋₁ mmHg₋₁ (P < 0.001). Interestingly, CalfBF (1.8±0.2 vs. 2.8±0.3mlmin₋₁ (100 g)₋₁) and CalfVC (2.0±0.3 vs. 3.9±0.5mlmin₋₁ (100 g)₋₁ mmHg₋₁ ×100) were also increased by this perturbation (P <0.05 for both). Infusion of PE and BHT-933 resulted in greater absolute decreases in FVC during leg heating compared to normothermic conditions (maximal decreases in FVC during heating vs. normothermia: PE: 7.8 ± 1.1 vs. 2.8 ± 0.5 ml min₋₁ mmHg₋₁; BHT-933: 8.6 ± 1.7 vs. 2.1 ± 0.4 ml min₋₁ mmHg₋₁; P < 0.01 for both). However, the nadir FVC during drug infusion was higher during passive leg heating compared to normothermic conditions (FVC at highest dose of respective drugs during heating vs. normothermic conditions: PE: 3.7 ± 0.4 vs. 2.0 ± 0.3 ml min₋₁ mmHg₋₁; BHT-933: 3.8 ± 0.2 vs. 2.1 ± 0.3 ml min₋₁ mmHg₋₁; P < 0.001 for both). Leg heating did not alter the responsiveness of CalfBF or CalfVC to either PE or BHT-933. Taken together, these observations suggest that local heating does not decrease α-adrenergic responsiveness.However, heat-induced vasodilatation opposes α-adrenergic vasoconstriction. Furthermore, passive heating of a limb causes not only an increase in skin blood flow but also in muscle blood flow.