Our previous study (27) showed that the cardiac sympathetic afferent reflex
(CSAR) was enhanced in dogs with congestive heart failure. The aim of this
study was to test whether blood volume expansion, which is one characteris
tic of congestive heart failure, potentiates the CSAR in normal dogs. Ten d
ogs were studied with sino-aortic denervation and bilateral cervical vagoto
my. Arterial pressure, left ventricular pressure, left ventricular epicardi
al diameter, heart rate, and renal sympathetic nerve activity were measured
. Coronary blood flow was also measured and, depending on the experimental
procedure, controlled. Blood volume expansion was carried out by infusion o
f isosmotic dextran into a femoral vein at 40 ml/kg at a rate of 50 ml/min.
CSAR was elicited by application of bradykinin (5 and 50 mug) and capsaici
n (10 and 100 mug) to the epicardial surface of the left ventricle. Volume
expansion increased arterial pressure, left ventricular pressure, left vent
ricular diameter, and coronary blood flow. Volume expansion without control
led coronary blood flow only enhanced the RSNA response to the high dose (5
0 mg) of epicardial bradykinin (17.3 +/- 1.9 vs. 10.6 +/- 4.8%, P< 0.05). H
owever, volume expansion significantly enhanced the RSNA responses to all d
oses of bradykinin and capsaicin when coronary blood flow was held at the p
revolume expansion level. The RSNA responses to bradykinin (16.9 +/- 4.1 vs
. 5.0 +/- 1.3% for 5 mg, P< 0.05, and 28.9 +/- 3.7 vs. 10.6 +/- 4.8% for 50
mg, P< 0.05) and capsaicin (29.8 +/- 6.0 vs. 9.3 +/- 3.1% for 10 mg, P< 0.
05, and 34.2 +/- 2.7 vs. 15.1 +/- 2.7% for 100 mug, P< 0.05) were significa
ntly augmented. These results indicate that acute volume expansion potentia
ted the CSAR. These data suggest that enhancement of the CSAR in congestive
heart failure may be mediated by the concomitant cardiac dilation, which a
ccompanies this disease state.