Naslov
Exercise attenuates alpha-adrenergic-receptor responsiveness in skeletal muscle vasculature

Autori
Buckwalter, John B. ; Naik, Jay S. ; Valić, Zoran ; Clifford, Philip S.

Izvornik
Journal of Applied Physiology (8750-7587) 90 (2001), 1; 172-178

Vrsta, podvrsta i kategorija rada
Radovi u časopisima, članak, znanstveni

Ključne riječi
blood flow; sympatholysis; autonomic nervous system; dogs; vasoconstriction

Sažetak
Attenuation of sympathetic vasoconstriction (sympatholysis) in working muscles during dynamic exercise is controversial. A potential mechanism is a reduction in -adrenergic-receptor responsiveness. The purpose of this study was to examine 1- and 2-adrenergic-receptor-mediated vasoconstriction in resting and exercising skeletal muscle using intra-arterial infusions of selective agonists. Thirteen mongrel dogs were instrumented chronically with flow probes on the external iliac arteries of both hindlimbs and a catheter in one femoral artery. The selective 1-adrenergic agonist (phenylephrine) or the selective 2-adrenergic agonist (clonidine) was infused as a bolus into the femoral artery catheter at rest and during mild and heavy exercise. Intra-arterial infusions of phenylephrine elicited reductions in vascular conductance of 76 ą 4, 71 ą 5, and 31 ą 2% at rest, 3 miles/h, and 6 miles/h and 10% grade, respectively. Intra-arterial clonidine reduced vascular conductance by 81 ą 5, 49 ą 4, and 14 ą 2%, respectively. The response to intra-arterial infusion of clonidine was unaffected by surgical sympathetic denervation. Agonist infusion did not affect either systemic blood pressure, heart rate, or blood flow in the contralateral iliac artery. 1-Adrenergic-receptor responsiveness was attenuated during heavy exercise. In contrast, 2-adrenergic-receptor responsiveness was attenuated even at a mild exercise intensity. These results suggest that the mechanism of exercise sympatholysis may involve reductions in postsynaptic -adrenergic-receptor responsiveness.

Izvorni jezik
Engleski

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