Cardiac receptors in ducks: the effect of their stimulation and blockade on diving bradycardia

Abstract

Cardiac receptors, activated by the rise in cardiac filling pressure during diving, evidently make a crucial contribution to diving bradycardia in the duck. The effects of receptor stimulation and blockade performed pharmacologically by injecting nicotine and lidocaine, respectively, into the pericardial sac were presented as supporting evidence. Nicotine activates epicardial receptors, causing transient bradycardia and hypotension, and increases in left ventricular diastolic pressure (LVDP) during diving can enhance bradycardia. Intrapericardial injection of 0.1% lidocaine sufficient to block the response of epicardial receptors to nicotine had no effect on diving bradycardia. Preventing LVDP rising, by continuous withdrawal of blood from the great veins during diving, also had no effect on the initiation or maintenance of bradycardia. A 0.5% solution of lidocaine injected intrapericardially caused an immediate increase in heart rate, even during vagal stimulation in a bilaterally vagotomized duck, and considerably reduced diving bradycardia in intact ducks. Evidence linking cardiac receptors to diving bradycardia was not confirmed. Cardiac receptors are not normally involved in the cardiac chronotropic response to diving.