TY - JOUR
T1 - Reflex α-adrenergic coronary vasoconstriction during hindlimb static exercise in dogs
AU - Aung-Din, R.
AU - Mitchell, J. H.
AU - Longhurst, J. C.
PY - 1981
Y1 - 1981
N2 - We studied 18 α-chloralose-anesthetized dogs to determine if α-adrenergic coronary vasoconstriction occurs with hindlimb static exercise. Exercise was elicited by spinal cord ventral nerve root stimulation. Regional coronary blood flow was determined by the radioactive microsphere method. Animals were studied under four experimental conditions: control rest and static exercise, rest and static exercise after β-adrenergic blockade with propranolol (2 mg/kg), rest and exercise after α-adrenergic blockade with phentolamine (.35 mg/kg), and rest and exercise after combined α- and β-adrenergic blockade. Myocardial oxygen consumption during exercise was determined during control and during α-adrenergic blockade conditions. Control hindlimb static exercise resulted in significant increases in systolic (10.6%) and diastolic (12.5%) arterial pressures, heart rate (12.2%), and double product (24.6%). Associated with the increased demand for oxygen, myocardial oxygen consumption increased (33.6%) as did left ventricular myocardial flow (29.6%). However, left ventricular coronary vascular resistance was unchanged during static exercise. After β-adrenergic blockade, systolic (12.2%) and diastolic (11.6%) arterial pressures and double product (10.7%) still increased significantly, but heart rate did not change with static exercise. In contrast, α-adrenergic vasoconstriction was unmasked as left (LV) and right (RV) ventricular myocardial blood flow decreased (LV: -30.0%, RV: -25.0%) and coronary vascular resistance increased (LV: 52.5%, RV: 45.3%) with static exercise. Combined α- and β-adrenergic blockade abolished the reduction in myocardial blood flow and the increase in coronary vascular resistance which occurred with static exercise after β-adrenergic blockade. These data suggest that, during static exercise, reflexes from skeletal muscles can cause α-adrenergic coronary artery vasoconstriction.
AB - We studied 18 α-chloralose-anesthetized dogs to determine if α-adrenergic coronary vasoconstriction occurs with hindlimb static exercise. Exercise was elicited by spinal cord ventral nerve root stimulation. Regional coronary blood flow was determined by the radioactive microsphere method. Animals were studied under four experimental conditions: control rest and static exercise, rest and static exercise after β-adrenergic blockade with propranolol (2 mg/kg), rest and exercise after α-adrenergic blockade with phentolamine (.35 mg/kg), and rest and exercise after combined α- and β-adrenergic blockade. Myocardial oxygen consumption during exercise was determined during control and during α-adrenergic blockade conditions. Control hindlimb static exercise resulted in significant increases in systolic (10.6%) and diastolic (12.5%) arterial pressures, heart rate (12.2%), and double product (24.6%). Associated with the increased demand for oxygen, myocardial oxygen consumption increased (33.6%) as did left ventricular myocardial flow (29.6%). However, left ventricular coronary vascular resistance was unchanged during static exercise. After β-adrenergic blockade, systolic (12.2%) and diastolic (11.6%) arterial pressures and double product (10.7%) still increased significantly, but heart rate did not change with static exercise. In contrast, α-adrenergic vasoconstriction was unmasked as left (LV) and right (RV) ventricular myocardial blood flow decreased (LV: -30.0%, RV: -25.0%) and coronary vascular resistance increased (LV: 52.5%, RV: 45.3%) with static exercise. Combined α- and β-adrenergic blockade abolished the reduction in myocardial blood flow and the increase in coronary vascular resistance which occurred with static exercise after β-adrenergic blockade. These data suggest that, during static exercise, reflexes from skeletal muscles can cause α-adrenergic coronary artery vasoconstriction.
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U2 - 10.1161/01.RES.48.4.502
DO - 10.1161/01.RES.48.4.502
M3 - Article
C2 - 6109582
AN - SCOPUS:0019422440
SN - 0009-7330
VL - 48
SP - 502
EP - 509
JO - Circulation research
JF - Circulation research
IS - 4
ER -