FEMORAL ARTERIAL INJECTION OF ADENOSINE IN HUMANS ELEVATES MSNA VIA CENTRAL BUT NOT PERIPHERAL MECHANISMS

Citation
Da. Maclean et al., FEMORAL ARTERIAL INJECTION OF ADENOSINE IN HUMANS ELEVATES MSNA VIA CENTRAL BUT NOT PERIPHERAL MECHANISMS, Journal of applied physiology, 83(4), 1997, pp. 1045-1053
Citations number
25
Categorie Soggetti
Physiology,"Sport Sciences
ISSN journal
87507587
Volume
83
Issue
4
Year of publication
1997
Pages
1045 - 1053
Database
ISI
SICI code
8750-7587(1997)83:4<1045:FAIOAI>2.0.ZU;2-5
Abstract
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 adenos ine 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 tim e of injection. The systemic infusion of phenylephrine resulted in an increase (P < 0.05) in mean arterial pressure of similar to 10 mmHg an d a decrease (P < 0.05) in heart rate of 8 - 10 beats/min compared wit h baseline values before phenylephrine infusion. After adenosine injec tion, the onset latency for the increase in MSNA was delayed to 19.2 /- 2.1 s and the magnitude of increase was attenuated by similar to 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 vari ables. 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 mag nitude of increase (276 +/- 28 U/min) was similar to that observed for adenosine alone. These data suggest that similar to 50% of the effect s of exogenously administered adenosine are a result of baroreceptor u nloading due to a drop in blood pressure. Furthermore, the finding tha t adenosine did not directly result in an increase in MSNA while it wa s trapped in the leg but that it needed to be released into the circul ation suggests that adenosine does not directly stimulate thin fiber m uscle afferents in the leg of humans. In contrast, it would appear tha t adenosine exerts its effects via some other chemically sensitive poo l of afferents.