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Copenhagen Muscle Research Center, Rigshospitalet, DK-2200 Copenhagen N, Denmark; and Division of Cardiology, The Milton S. Hershey Medical Center, The Pennsylvania State University, Hershey, Pennsylvania 17033
Received 1 April 1997; accepted in final form 11 June 1997.
MacLean, D. A., B. Saltin, G. Rådegran, and L. Sinoway. Femoral arterial injection of adenosine in humans
elevates MSNA via central but not peripheral mechanisms.
J. Appl. Physiol. 83(4):
1045-1053, 1997.
The purpose of the present study was to examine
the effects of femoral arterial injections of adenosine on muscle
sympathetic nerve activity (MSNA) under three different conditions.
These conditions were adenosine injection alone, adenosine injection
after phenylephrine infusion, and adenosine injection distal to a thigh
cuff inflated to arrest the circulation. The arterial injection of
adenosine alone resulted in a fourfold (255 ± 18 U/min) increase
above baseline (73 ± 12 U/min; P < 0.05) in MSNA with an onset latency of 15.8 ± 0.8 s from the
time of injection. The systemic infusion of phenylephrine resulted in an increase (P < 0.05) in mean
arterial pressure of ~10 mmHg and a decrease
(P < 0.05) in heart rate of
8-10 beats/min compared with baseline values before phenylephrine
infusion. After adenosine injection, the onset latency for the increase
in MSNA was delayed to 19.2 ± 2.1 s and the magnitude of increase
was attenuated by ~50% (123 ± 20 U/min) compared with adenosine
injection alone (P < 0.05). When a
cuff was inflated to 220 mmHg to arrest the circulation and adenosine
was injected into the leg distal to the inflated cuff, there were no
significant changes in MSNA or any of the other measured variables.
However, on deflation of the cuff, there was a rapid increase
(P < 0.05) in MSNA, with an onset
latency of 9.1 ± 0.9 s, and the magnitude of increase (276 ± 28 U/min) was similar to that observed for adenosine alone. These data
suggest that ~50% of the effects of exogenously administered adenosine are a result of baroreceptor unloading due to a drop in blood
pressure. Furthermore, the finding that adenosine did not directly
result in an increase in MSNA while it was trapped in the leg but that
it needed to be released into the circulation suggests that adenosine
does not directly stimulate thin fiber muscle afferents in the leg of
humans. In contrast, it would appear that adenosine exerts its effects
via some other chemically sensitive pool of afferents.
muscle sympathetic nerve activity; discharge; injection
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