Cardiac receptors in ducks--a link between vasoconstruction and bradycardia during diving

It has been demonstrated that cardiac receptors, most likely of the left ventricular type, are present also in the duck's heart. These receptors and their reflex responses (i.e. bradycardia and hypotension) could be blocked by intrapericardial administration of lidocaine. Initially, usch receptor blockade did not affect efferent vagal control of heart rate, as revealed by undiminished bradycardia in response to a standardized vagal stimulation. After cardiac receptor blockade, however, the duck's normal bradycardia response to head immersion was greatly reduced. The cardiovascular response to submersion was now instead characterized by a marked rise in arterial pressure, with superimposed bouts of intensified bradycardia and pressure reduction, evidently induced reflexly from the arterial baroreceptors. Meanwhile, the bradycardia response to standarized efferent vagal stimulation was still the same as before intrapericardial lidocaine injection. These results suggest that the marked rise in cardiac filling pressure following the intense shemo-receptor-induced constriction of both resistance and capacitance vessels, activates ventricular stretch receptors signalling in vagal afferents. Apparently, the activation of these receptors contributes crucially to the bradycardia and reduction of cardial output, which balance off the greatly increased peripheral resistance in the diving duck.