AJP - Heart and Circulatory Physiology, Vol 243, Issue 5 815-H818, Copyright © 1982 by American Physiological Society
Sensitization of vagal cardiopulmonary baroreflex by chronic digoxin
M. D. Thames, B. D. Miller and F. M. Abboud
It has been recently reported that intracoronary acetylstrophanthidin
injection acutely sensitizes the cardiac baroreflex (vagal afferents). We
wondered whether chronic administration of digoxin also augmented the gain
of this reflex. We treated seven dogs with digoxin intravenously (40
micrograms/kg loading dose followed by 15 micrograms.kg-1.day-1) for 7
days; eight additional dogs received vehicle for 7 days. With the dogs
under chloralose anesthesia, we assessed the changes in renal nerve
activity that resulted from stimulation of cardiopulmonary receptors with
volume expansion (15 ml/kg of 6% dextran in saline) in digoxin- and
vehicle-treated groups under control conditions, after sinoaortic
denervation (SAD), and after SAD plus vagotomy. Under control conditions
volume expansion resulted in decreases of renal nerve activity of 13.5 +/-
3.5%/mmHg increase in pulmonary artery wedge pressure in digoxin-treated
dogs. This tended to be greater than the response of sham-treated dogs
(-9.5 +/- 1.5%/mmHg increase). After SAD, renal nerve activity decreased 19
+/- 5%/mmHg increase in pulmonary artery wedge pressure in the digoxin
group compared with only 8 +/- 1%/mmHg increase in the vehicle group. These
responses were significantly different. The plasma digoxin level in the
digoxin-treated group was in the therapeutic range (1.9 +/- 0.4 ng/ml).
Vagotomy abolished the responses to volume expansion in both groups. Thus
chronic digoxin treatment resulting in therapeutic plasma levels of digoxin
sensitizes vagal afferents mediating the cardiopulmonary baroreflex
influence on renal nerve activity.
