Author + information
- Received October 31, 1985
- Revision received May 12, 1986
- Accepted June 20, 1986
- Published online January 1, 1987.
- ↵*Address for reprints: Marc D. Thames, MD, Chief, Cardiology Section (111J), McGuire Veterans Administration Medical Center, 1201 Broad Rock Boulevard, Richmond, Virginia 23249.
Ventricular arrhythmias generally result in a decrease in arterial pressure and increases in atrial and ventricular filling pressures which would be expected to induce reflex changes in efferent sympathetic nerve activity to the heart and peripheral circulation. Experiments were performed in 14 anesthetized dogs in order to 1) determine whether programmed ventricular stimulation produces changes in renal sympathetic nerve activity; 2) quantitate these changes; and 3) determine the cardiovascular reflexes that mediate these changes. Arterial and right atrial pressures and renal sympathetic nerve activity were recorded in dogs before and after administration of single and double programmed ventricular stimuli.
In a group of 10 dogs after single extrastimuli, diastolic arterial pressure decreased by 18 ± 2 mm Hg (mean ± SEM) while renal sympathetic nerve activity increased by 39 ± 15 impulses/s. These changes were directly related to degree of stimulus prematurity. After double extrastimuli, diastolic arterial pressure decreased by 22 ± 2 mm Hg whereas renal sympathetic activity increased by 55 ± 8 impulses/s. In an additional four dogs, double extrastimuli decreased arterial pressure (−34 ± 1 mm Hg) and increased cardiac (86 ± 16%) and renal (82 ± 12%) sympathetic traffic. After si-noaortic denervation, neither single nor double programmed ventricular stimuli resulted in alterations in cardiac or renal sympathetic nerve activity. It is concluded that the decreased arterial pressure caused by single and double programmed ventricular stimuli leads to increases in cardiac and renal sympathetic nerve activity that are mediated by sinoaortic baroreflexes.
- Received October 31, 1985.
- Revision received May 12, 1986.
- Accepted June 20, 1986.
- American College of Cardiology