By stimulating afferent nerve endings in skeletal muscle, heart, kidney and
the carotid body, adenosine infusion evokes a receptor-specific sympatho-e
xcitatory reflex in humans that overrides its direct negative chronotropic
effect. We tested the hypothesis that adenosine increases heart rate by sup
pressing parasympathetic and augmenting sympathetic components of heart rat
e variability. High-frequency (P-H; 0. 15-0.50 Hz) and low-frequency (P-L;
0.05-0.15 Hz) components of heart rate variability total power (PT) Were de
termined by spectral analysis. The ratios P-H/P-T and P-L/P-H respectively
were used to estimate parasympathetic and sympathetic input to the sino-atr
ial node. Heart rate was recorded before and during a 5 min intravenous inf
usion of adenosine (140 mu g.min(-1) kg(-1)) in seven healthy men. Adenosin
e did not affect blood pressure, but increased heart rate by 33 +/- 6 beats
/min, and reduced P-T P-H P-L and P-H/P-T. In contrast, there was an increa
se in P-L/P-H. In a second experiment in nine men, brachial artery infusion
of adenosine (15 mu g.min(-1) 100 ml(-1) forearm tissue) increased heart r
ate by 3 beats/min, had no effect on P-T, P-H, P(L)or P-H/P-T, yet increase
d P-L/P-H. Intra-arterial adenosine exerts a modest effect on heart rate by
modulating cardiac sympathetic indices, without affecting parasympathetic
indices, of heart rate variability, whereas intravenous infusion of adenosi
ne reduces heart rate variability and raises heart rate by decreasing paras
ympathetic and increasing cardiac sympathetic tone. These reflex effects ma
y become clinically relevant during adenosine stress testing, or when endog
enous adenosine is increased, such as during ischaemia, exercise or vasodep
ressor reactions, or in heart failure.