Increased cardiac sympathetic nerve activity in heart failure is not due to desensitization of the arterial baroreflex

• Published in: American journal of physiology. Heart and circulatory physiology Vol. 293; no. 1; pp. H798 - H804
• Main Authors: Watson, A. M. D, Hood, S. G, Ramchandra, R, McAllen, R. M, May, C. N
• Format: Journal Article
• Language: English
• Published: United States American Physiological Society 01.07.2007
• Subjects: Animals; Arteries - physiopathology; Baroreflex; Blood Pressure; Cardiac Output, Low - physiopathology; Coronary vessels; Female; Heart failure; Heart Rate; Medical prognosis; Reflexes; Sheep; Sympathetic Nervous System - physiopathology
• ISSN: 0363-6135; 1522-1539
• DOI: 10.1152/ajpheart.00147.2007

Howard Florey Institute, University of Melbourne, Victoria 3010, Australia Submitted 6 February 2007 ; accepted in final form 5 April 2007 Increased sympathetic drive to the heart worsens prognosis in heart failure, but the level of cardiac sympathetic nerve activity (CSNA) has been assessed only by indirect methods, which do not permit testing of whether its control by arterial baroreceptors is defective. To do this, CSNA was measured directly in 16 female sheep, 8 of which had been ventricularly paced at 200–220 beats/min for 4–6 wk, until their ejection fraction fell to between 35 and 40%. Recording electrodes were surgically implanted in the cardiac sympathetic nerves, and after 3 days' recovery the responses to intravenous phenylephrine and nitroprusside infusions were measured in conscious sheep. Electrophysiological recordings showed that resting CSNA (bursts/100 heartbeats) was significantly elevated in heart-failure sheep (89 ± 3) compared with normal animals (46 ± 6; P < 0.001). This increased CSNA was not accompanied by any increase in the low-frequency power of heart-rate variability. The baroreceptor-heart rate reflex was significantly depressed in heart failure (maximum gain –3.29 ± 0.56 vs. –5.34 ± 0.66 beats·min –1 ·mmHg –1 in normal animals), confirming published findings. In contrast, the baroreflex control of CSNA was undiminished (maximum gain in heart failure –6.33 ± 1.06 vs. –6.03 ± 0.95%max/mmHg in normal sheep). Direct recordings in a sheep model of heart failure thus show that resting CSNA is strikingly increased, but this is not due to defective control by arterial baroreceptors. baroreceptors; pacing; spectral analysis Address for reprint requests and other correspondence: C. N. May, Howard Florey Institute, Univ. of Melbourne, Parkville, Vic 3010, Australia (e-mail: clive.may{at}florey.edu.au )