R. Bergeron et al., Splanchnic blood flow and hepatic glucose production in exercising humans:role of renin-angiotensin system, AM J P-REG, 281(6), 2001, pp. R1854-R1861
Citations number
34
Categorie Soggetti
Physiology
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
The study examined the implication of the renin-angiotensin system (RAS) in
regulation of splanchnic blood flow and glucose production in exercising h
umans. Subjects cycled for 40 min at 50% maximal O-2 consumption ((V) over
dot O-2 (max)) followed by 30 min at 70% (V) over dot O-2 max either with [
angiotensin-converting enzyme (ACE) blockade] or without (control) administ
ration of the ACE inhibitor enalapril (10 mg iv). Splanchnic blood flow was
estimated by indocyanine green, and splanchnic substrate exchange was dete
rmined by the arteriohepatic venous difference. Exercise led to an similar
to 20-fold increase (P < 0.001) in ANG II levels in the control group (5.4
+/- 1.0 to 102.0 +/- 25.1 pg/ml), whereas this response was blunted during
ACE blockade (8.1 +/- 1.2 to 13.2 +/- 2.4 pg/ml) and in response to an orth
ostatic challenge performed postexercise. Apart from lactate and cortisol,
which were higher in the ACE-blockade group vs. the control group, hormones
, metabolites, (V) over dot O-2, and RER followed the same pattern of chang
es in ACE-blockade and control groups during exercise. Splanchnic blood flo
w (at rest: 1.67 +/- 0.12, ACE blockade; 1.59 +/- 0.18 l/min, control) decr
eased during moderate exercise (0.78 +/- 0.07, ACE blockade; 0.74 +/- 0.14
l/min, control), whereas splanchnic glucose production (at rest: 0.50 +/- 0
.06, ACE blockade; 0.68 +/- 0.10 mmol/min, control) increased during modera
te exercise (1.97 +/- 0.29, ACE blockade; 1.91 +/- 0.41 mmol/min, control).
Refuting a major role of the RAS for these responses, no differences in th
e pattern of change of splanchnic blood flow and splanchnic glucose product
ion were observed during ACE blockade compared with controls. This study de
monstrates that the normal increase in ANG II levels observed during prolon
ged exercise in humans does not play a major role in the regulation of spla
nchnic blood flow and glucose production.