|
|
||||||||
AJP - Regulatory, Integrative and Comparative Physiology, Vol 255, Issue 4 654-R664, Copyright © 1988 by American Physiological Society
ARTICLES |
M. Weinstock, P. I. Korner, G. A. Head and P. K. Dorward
Baker Medical Research Institute, Melbourne, Victoria, Australia.
Sigmoidal mean arterial pressure (MAP)-heart rate (HR) curves were obtained in two genetically related strains of rabbits (groups I and II). We examined vagal (V) and sympathetic (S) effects on HR using perivascular cuffs and vasoactive drugs to alter MAP, and we studied the effects of intravenous naloxone, which affected only I. With the cuff method, both V and S components of gain were much greater in I than in II, and naloxone greatly reduced the difference. With the drug method, gain was similar in I and II and unaffected by naloxone. With both methods, the V component of HR range between plateaus was greater in I than in II because of more pronounced bradycardia at the lower plateau; naloxone eliminated the latter difference when the reflex was drug induced but not when it was cuff induced. The S component of HR range was similar in I and II; with both methods, the tachycardia plateau was reduced by naloxone. The cuff method alters cardiac load more than the drug method, leading to engagement of different groups of afferents for a given change in MAP (delta MAP). We have derived an input-output model, which suggests that with the drug method, gain is almost entirely determined by the input from the arterial baroreceptors, accounting for the minimal difference between I and II. With the cuff method, gain is determined by a nonlinear interaction involving the arterial and nonarterial baroreceptors, which accentuates the response. The opiate mechanism is associated with the nonarterial baroreceptor input and has amplifying properties, which account for the difference in gain between I and II. The two methods and naloxone provide a novel way of differentiating the effector patterns of the reflex; naloxone serves as a marker of activity in a particular pathway.
This article has been cited by other articles:
![]() |
D. L. Daubert, D. Liu, I. H. Zucker, and V. L. Brooks Roles of nitric oxide and angiotensin II in the impaired baroreflex gain of pregnancy Am J Physiol Regulatory Integrative Comp Physiol, June 1, 2007; 292(6): R2179 - R2187. [Abstract] [Full Text] [PDF] |
||||
![]() |
X. Ma, F. M. Abboud, and M. W. Chapleau Analysis of afferent, central, and efferent components of the baroreceptor reflex in mice Am J Physiol Regulatory Integrative Comp Physiol, November 1, 2002; 283(5): R1033 - R1040. [Abstract] [Full Text] [PDF] |
||||
![]() |
V. L. Brooks, K. A. Clow, and K. P. O'Hagan Pregnancy and acute baroreflex resetting in conscious rabbits Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2002; 283(2): R429 - R440. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. Gaudet, S. J. Godwin, and G. A. Head Effects of central infusion of ANG II and losartan on the cardiac baroreflex in rabbits Am J Physiol Heart Circ Physiol, February 1, 2000; 278(2): H558 - H566. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. H. Ricketts and G. A. Head A five-parameter logistic equation for investigating asymmetry of curvature in baroreflex studies Am J Physiol Regulatory Integrative Comp Physiol, August 1, 1999; 277(2): R441 - R454. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. C. Malpas, A. S. Groom, and G. A. Head Baroreflex Control of Heart Rate and Cardiac Hypertrophy in Angiotensin II–Induced Hypertension in Rabbits Hypertension, June 1, 1997; 29(6): 1284 - 1290. [Abstract] [Full Text] |
||||
![]() |
C. J. Thomas, A. J. Rankin, G. A. Head, and R. L. Woods ANP Enhances Bradycardic Reflexes in Normotensive but Not Spontaneously Hypertensive Rats Hypertension, May 1, 1997; 29(5): 1126 - 1132. [Abstract] [Full Text] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |