Forearm blood flow (FBF) was measured during brachial artery infusions of acetylcholine (ACh), to evoke endothelial NO release, and the NO donor nitroprusside (NTP), in 5 healthy volunteers. Sympathetic activity was increased by lower body suction and antagonized by brachial infusion of phentolamine. In the control condition, FBF was 2.4±0.4 mI·100 ml·min-1' and rose by 16.9±3.6 ml·100 ml·min-1 during ACh at 16 ug·min"1 and by 17.0±4.3 ml·100 ml·min-1 at 64 ng·min-1. With suction, FBF was 1.7±0.6 ml·100ml·min-1 (p<0.05 vs control) and rose by 11.4±3.2 ml·100 ml·min-1 during ACh at 16 ng·min-1 (p<0.05 vs control) and by 12.2±3.8 ml·100 ml·min-1 at 64 ug·min-1 (p=0.08 vs control). After phentolamine, FBF was 3.8±0.5 at baseline (p<0.05 vs control) and the increases in flow with ACh at both 16 and 64 μg·min-1 were identical to control. Similar resting values were observed prior to NTP infusions. FBF rose 6.3±1.1 ml·100 ml·min-1 with NTP at 2.5 ng·min-1 and by 12.1±1.4 ml·100ml·min-1 at 10 ng·min-1. Suction blunted and phentolamine augmented the increases in flow with NTP by ∼50% (p<0.05). The effects of altered sympathetic activity on the blood flow responses to NTP suggest that sympathetic activity modulates NO-mediated vasodilation. The less consistent effects on ACh-mediated vasodilation suggests that vasodilating mechanisms, in addition to NO, can be activated by ACh administration to the human forearm.
|Original language||English (US)|
|State||Published - Dec 1 1996|
ASJC Scopus subject areas
- Molecular Biology