A growing body of evidence suggests that the cardiac glycosides exert part of their action by virtue of their neuroexcitatory effects. The present study was undertaken to examine the effects of ouabain on the discharge from left atrial stretch receptors. Single unit activity was recorded from the left cervical vagus of chloralose anesthetized dogs. Left atrial pressure was elevated by the i.v. infusion of isotonic saline. In 7 dogs, 2 control volume expansions were followed by the i.v. injection of ouabain octahydrate (20 μg/kg). Left atrial pressure was again increased by volume expansion 10 min after ouabain administration. Hemodynamic parameters and atrial receptor discharge were recorded after each aliquot of volume (25-50 ml) was administered. Before volume expansion, ouabain significantly increased atrial receptor discharge (8.7 ± 1.3 spikes per cardiac cycle to a maximum of 15.6 ± 3.5 spikes per cardiac cycle; P < .05) as early as 2 min after injection. There were no significant changes in heart rate, left atrial pressure or mean arterial pressure. Sequential volume expansions tended to decrease atrial receptor sensitivity in control animals. Therefore, 3 dogs served as time controls and the 3rd and 4th volume expansions after the vehicle administration were compared to the 3rd and 4th volume expansions after ouabain administration. The relationship between left atrial pressure and receptor discharge in terms of spikes per cardiac cycle were plotted. When compared to the control volume expansions, there was a significant increase in the slope of the lines relating increase in atrial receptor discharge to increase in left atrial pressure. The present studies indicate that ouabain can increase the sensitivity of left atrial stretch receptors.
|Original language||English (US)|
|Number of pages||5|
|Journal||Journal of Pharmacology and Experimental Therapeutics|
|State||Published - Jan 1 1980|
ASJC Scopus subject areas
- Molecular Medicine