Increased left ventricular pressure attenuates the baroreflex in unanesthetized dogs

To determine whether stimulation of left ventricular mechanoreceptors alters the baroreflex control of heart rate (HR), dogs were instrumented with a vascular occluder around the ascending aorta and appropriate instrumentation for the recording of left ventricular pressure (LVP), aortic pressure, left atrial pressure, HR, and left ventricular dP/dt. Baroreflex sensitivity (pulse interval or HR vs. aortic systolic pressure linear-regression slopes to infusions of phenylephrine or nitroprusside) was determined in the conscious state a minimum of 7 days postoperatively. After control responses were determined with both phenylephrine and nitroprusside, the experiment was repeated during inflation of the ascending aortic occluder so as to significantly raise left ventricle systolic pressure from 127.9 ± 8.4 to 178.5 ± 11.3 mmHg (P<0.01) and left ventricle end-diastolic pressure from 3.5 ± 0.7 to 8.9 ± 1.0 mmHg (P<0.01). There were no changes in mean arterial blood pressure, pulse pressure, or HR during elevation of LVP. The baroreflex sensitivity was reduced only during the infusion of nitroprusside from a control of 11.03 ± 1.9 to 4.80 ± 1.2 ms/mmHg (P<0.01) for the pulse interval relationship and from -2.51 ± 0.53 to -1.14 ± 0.32 beats.min^-1.mmHg^-1 (P<0.05) for the HR relationship. Cholinergic blockade with atropine abolished the depression in the baroreflex sensitivity during nitroprusside infusion when LVP was increased. β₁-Adrenergic blockade with metoprolol did not significantly reduce the baroreflex sensitivity during increased LVP. We conclude from these data that distension of the left ventricle within a physiological range of pressures depresses the baroreflex control of HR in the conscious dog and that this depression is primarily mediated by a reduction in vagal efferent withdrawal during baroreceptor unloading.