Nitric oxide in the regulation of vasomotor tone in human skeletal muscle

Citation
G. Radegran et B. Saltin, Nitric oxide in the regulation of vasomotor tone in human skeletal muscle, AM J P-HEAR, 45(6), 1999, pp. H1951-H1960
Citations number
30
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
ISSN journal
03636135 → ACNP
Volume
45
Issue
6
Year of publication
1999
Pages
H1951 - H1960
Database
ISI
SICI code
0363-6135(199906)45:6<H1951:NOITRO>2.0.ZU;2-3
Abstract
The role of nitric oxide (NO) as a regulator of vasomotor tone has been inv estigated in resting and exercising human skeletal muscle. At rest, NO synt hase (NOS) inhibition by intraarterial infusion of N-G-monomethyl-L-arginin e decreased femoral artery blood flow (FABF, ultrasound Doppler) from 0.39 +/- 0.08 to 0.18 +/- 0.03 l/min (P < 0.01), i.e., by similar to 52%, and in creased leg O-2 extraction from 62.1 +/- 9.8 to 100.9 +/- 4.5 ml/l (P < 0.0 04); thus leg O-2 uptake ((V) over doto(2), 22 +/- 4 ml/min, similar to 0.7 5 ml.min(-1).100 g(-1)) was unaltered [not significant (P = NS)]. Mean arte rial pressure (MAP) increased by 8 +/- 2 mmHg (P < 0.01). Heart rate (HR, 5 3 +/- 3 beats/min) was unaltered (P = NS). The NOS inhibition had, however, no effect on the initial rate of rise or the magnitude of FABF (4.8 +/- 0. 4 l/min, similar to 163 ml.min(-1).100 g(-1)), MAP (117 +/- 3 mmHg), HR (98 +/- 5 beats/min), or leg (V) over doto(2) (704 +/- 55 ml/min, similar to 2 4 ml.min(-1).100 g(-1), P = NS) during submaximal, one-legged, dynamic knee -extensor exercise. Similarly, FABF (7.6 +/- 1.0 l/min, similar to 258 ml.m in(-1).100 g(-1)), MAP (140 +/- 8 mmHg), and leg (V) over doto(2) (1,173 +/ - 139 ml/min, similar to 40 ml.min(-1).100 g(-1))were unaffected at termina tion of peak effort (P = NS). Peak HR (137 +/- 3 beats/min) was, however, l owered by 10% (P < 0.01). During recovery, NOS inhibition reduced FABF by s imilar to 34% (P < 0.04), which was compensated for by an increase in the l eg O-2 extraction by similar to 41% (P < 0.04); thus leg (V) over doto(2) w as unaltered (P = NS). In conclusion, these findings indicate that NO is no t essential for the initiation or maintenance of active hyperemia in human skeletal muscle but support a role for NO during rest, including recovery f rom exercise. Moreover, changes in blood flow during rest and recovery caus ed by NOS inhibition are accompanied by reciprocal changes in O-2 extractio n, and thus (V) over doto(2) is maintained.