Increased right atrial pressure attenuates the bradycardic response to vagal stimulation in animal models, suggesting a physiological interaction in heart rate control.
Elevated right atrial pressure may blunt vagal bradycardia in animals; leaves open relevance to human heart rate control.
We have recently shown that the intrinsic rate response to an increase in right atrial pressure is augmented when cardiac muscarinic receptors are activated. This present study examines the cardiac pacemaker response to vagal stimulation at different values of right atrial pressure in isolated rat right atrium and in the rabbit heart in situ. In the rat atrium, when pressure was raised in steps from 2 to 10 mmHg, there was a progressive reduction in the response to vagal stimulation [40.5 +/- 7.2% reduction (mean +/- SE) at 8 mmHg, P < 0.01], which was independent of the level of vagal bradycardia, that persisted in the presence of the beta-adrenergic agonist isoproterenol. In barbiturate-anesthetized rabbits with cervical vagi cut and beta-adrenergic blockade, raising right atrial pressure approximately 2.5 mmHg by blood volume expansion reduced the bradycardia elicited by electrical stimulation of the peripheral end of the right vagus nerve (9.1 +/- 1.1% reduction, P < 0.0001). These results demonstrate that vagal bradycardia is modulated by the level of right atrial pressure and suggest that normally right atrial pressure may interact with cardiac vagal activity in the control of heart rate.
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Bolter et al. (1999) studied this question.
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