Dynamic exercise causes an increase in circulating blood levels of ren
in and vasopressin (AVP), yet the afferent mechanisms responsible for
release of renin and AVP during exercise are poorly understood. Partia
l ischemia of active skeletal muscle induces a reflex pressor response
, termed the muscle metaboreflex. Does muscle metaboreflex activation
induce release of renin and AVP? The muscle metaboreflex was activated
in conscious, chronically instrumented dogs during mild treadmill exe
rcise (3.2 km/h, 0% grade) via graded partial occlusion of terminal ao
rtic blood flow. Decreasing hindlimb perfusion to 40% of the control l
evel during exercise significantly increased systemic arterial pressur
e (SAP) and heart rate (HR) from 103.4 +/- 2.4 to 166.7 +/- 4.2 mmHg a
nd from 111.6 +/- 9.9 to 141.9 +/- 3.9 beats/min, respectively. Howeve
r, only small nonsignificant changes in arterial plasma renin activity
and AVP concentration occurred [control: renin = 0.46 +/- 0.8 ng angi
otensin I (ANG I) . ml-1 . h-1, AVP = 0.53 +/- 0.17 pg/ml; metaborefle
x activation: renin = 0.77 +/- 0.33 ng ANG I . ml-1 . h-1, AVP = 1.09
+/- 0.34 pg/ml]. The experiments were repeated after ganglionic blocka
de (hexamethonium 10 mg/ml and atropine 0.2 mg/ml iv) to attenuate the
reflex increase in SAP. In this setting, metaboreflex activation caus
ed SAP to increase from 91.6 +/- 4.3 to only 114.7 +/- 6.8 mmHg and th
e reflex tachycardia was abolished (153.7 +/- 5.8 to 159.3 +/- 6.1 bea
ts/min, P > 0.05). With the reflex pressor response markedly attenuate
d, AVP increased from 2.53 +/- 0.81 to 34.38 +/- 6.59 pg/ml with muscl
e metaboreflex activation, whereas no significant changes in renin act
ivity occurred. Thus, in the absence of a marked increase in SAP, meta
boreflex activation does induce the release of AVP. The lack of effect
of metaboreflex activation on AVP before ganglionic blockade is likel
y caused by arterial baroreflex suppression of activity in vasopressin
neurosecretory cells due to the large increase in SAP.