Rapid dilation of arterioles with single contraction of hamster skeletal muscle

Abstract

Skeletal muscle blood flow increases rapidly with exercise onset, but little is known of where or how the rapid onset of vasodilation (ROV) is governed within the microcirculation. In the retractor muscle of anesthetized hamsters ( n = 26), we tested the following: 1) where in the resistance network ROV occurred, 2) how microvascular responses were affected by the duration of contraction, and 3) whether ROV involved muscarinic receptor activation. Single tetanic contractions were evoked using supramaximal field stimulation (100 Hz) to depolarize motor end plates. In response to a 200-ms contraction, red blood cell (rbc) velocity ( Vrbc) in feed arteries (FA; rest: 17.8 ± 2 mm/s) increased within 1 s; a transient first peak (P1; 50 ± 7% increase) occurred at ∼5 s; and a second peak (P2; 50 ± 15% increase) occurred at ∼15–20 s. For vasodilation, P1 increased in frequency from proximal FA (2/7) and 1A arterioles (2/7) to distal 2A (4/7) and 3A (7/8) arterioles ( P < 0.05). Relative to resting (and maximal, 10 μM sodium nitroprusside) diameters, P1 increased from proximal (FA, 3 ± 2% from 57 ± 5 μm) to distal (3A, 27 ± 6% from 14 ± 1 μm) vessel branches ( P < 0.05). P2 was manifest in all vessels and increased relative to resting diameters from FA (11 ± 3%) to 3A (36 ± 6%) branches ( P < 0.01). Extending a contraction from 200 to 1,000 ms (tension × time integral from 17 ± 2 to 73 ± 4 mN/mm2 × s) increased P1 and P2 for Vrbc and for diameter ( P < 0.05) while reducing the time of onset for P2 ( P < 0.05). Superfusion with atropine (10 μM) attenuated P1 of vasodilation (200 ms contraction) from 26 ± 8% to 6 ± 2% ( n = 7 across branches; P < 0.05) and reduced the diameter × time integral by 46 ± 13% ( P < 0.05) without changing P2. We conclude that ROV in the hamster retractor muscle is initiated in distal arterioles, increases with the duration of muscle contraction, and involves muscarinic receptor activation.