TY - JOUR
T1 - α-adrenergic vasoconstriction in active skeletal muscles during dynamic exercise
AU - Buckwalter, John B.
AU - Clifford, Philip S.
PY - 1999/7
Y1 - 1999/7
N2 - Sympathetic vasoconstriction in working muscles during dynamic exercise has been demonstrated by intra-arterial administration of α1-adrenergic antagonists. The purpose of this study was to examine the existence of α1- and α2-adrenergic receptor-mediated vasoconstriction in active skeletal muscles during exercise. Six mongrel dogs were instrumented chronically with flow probes on the external iliac arteries of both hindlimbs, and a catheter was inserted in one femoral artery. All dogs ran on a motorized treadmill at three exercise intensities (3 miles/h, 6 miles/h, and 6 miles/h at 10% grade) on separate days. After 5 min of exercise, a selective α1- (prazosin) or a selective α2-adrenergic antagonist (rauwolscine) was infused as a bolus into the femoral arterial catheter (only one drug per day). The doses of the antagonists were adjusted to maintain the same effective concentration at each exercise intensity. At the mild, moderate, and heavy workloads prazosin infusion produced immediate increases in iliac conductance of 65 ± 9, 35 ± 6, and 18 ± 4% (means ± SE), respectively, and increases in blood flow of 290 ± 24, 216 ± 23, and 172 ± 18 ml/min, respectively. Rauwolscine infusion produced increases in conductance of 52 ± 5%, 36 ± 5%, and 26 ± 3%, respectively, and blood flow increases of 250 ± 34, 244 ± 39, and 259 ± 35 ml/min at the three workloads. Systemic blood pressure and blood flow in the contralateral iliac artery were unaffected by any of the antagonist infusions. These results demonstrate that there is ongoing α1- and α2- adrenergic receptor-mediated vasoconstriction in exercising skeletal muscles even at heavy workloads and that the magnitude of vasoconstriction decreases as exercise intensity increases.
AB - Sympathetic vasoconstriction in working muscles during dynamic exercise has been demonstrated by intra-arterial administration of α1-adrenergic antagonists. The purpose of this study was to examine the existence of α1- and α2-adrenergic receptor-mediated vasoconstriction in active skeletal muscles during exercise. Six mongrel dogs were instrumented chronically with flow probes on the external iliac arteries of both hindlimbs, and a catheter was inserted in one femoral artery. All dogs ran on a motorized treadmill at three exercise intensities (3 miles/h, 6 miles/h, and 6 miles/h at 10% grade) on separate days. After 5 min of exercise, a selective α1- (prazosin) or a selective α2-adrenergic antagonist (rauwolscine) was infused as a bolus into the femoral arterial catheter (only one drug per day). The doses of the antagonists were adjusted to maintain the same effective concentration at each exercise intensity. At the mild, moderate, and heavy workloads prazosin infusion produced immediate increases in iliac conductance of 65 ± 9, 35 ± 6, and 18 ± 4% (means ± SE), respectively, and increases in blood flow of 290 ± 24, 216 ± 23, and 172 ± 18 ml/min, respectively. Rauwolscine infusion produced increases in conductance of 52 ± 5%, 36 ± 5%, and 26 ± 3%, respectively, and blood flow increases of 250 ± 34, 244 ± 39, and 259 ± 35 ml/min at the three workloads. Systemic blood pressure and blood flow in the contralateral iliac artery were unaffected by any of the antagonist infusions. These results demonstrate that there is ongoing α1- and α2- adrenergic receptor-mediated vasoconstriction in exercising skeletal muscles even at heavy workloads and that the magnitude of vasoconstriction decreases as exercise intensity increases.
KW - Blood flow
KW - Dogs
KW - Rauwolscine
KW - Sympathetic nervous system
KW - α-adrenergic receptor
UR - http://www.scopus.com/inward/record.url?scp=0032865211&partnerID=8YFLogxK
U2 - 10.1152/ajpheart.1999.277.1.h33
DO - 10.1152/ajpheart.1999.277.1.h33
M3 - Article
C2 - 10409179
AN - SCOPUS:0032865211
SN - 0363-6135
VL - 277
SP - H33-H39
JO - American Journal of Physiology - Heart and Circulatory Physiology
JF - American Journal of Physiology - Heart and Circulatory Physiology
IS - 1 46-1
ER -