|
|
||||||||
AJP - Regulatory, Integrative and Comparative Physiology, Vol 269, Issue 3 678-R690, Copyright © 1995 by American Physiological Society
ARTICLES |
T. E. Lohmeier, G. A. Reinhart, H. L. Mizelle, J. P. Montani, R. Hester, C. E. Hord Jr and D. A. Hildebrandt
Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson 39216-4505, USA.
The purpose of this study was to elucidate the role of the renal nerves in promoting sodium retention during chronic reductions in cardiac output. In five dogs, the left kidney was denervated and the urinary bladder was surgically divided to allow separate 24-h urine collection from the innervated and denervated kidneys. Additionally, progressive reductions in cardiac output were achieved by employing an externally adjustable occluder around the pulmonary artery and by servo-controlling right atrial pressure (control = 0.9 +/- 0.2 mmHg) at 4.7 +/- 0.1, 7.5 +/- 0.1, and 9.8 +/- 0.2 mmHg for 3 days at each level. At the highest level of right atrial pressure, the 24-h values for mean arterial pressure (control = 97 +/- 3 mmHg) and cardiac output (control = 2,434 +/- 177 ml/min) were reduced approximately 25 and 55%, respectively; glomerular filtration rate fell by approximately 35% and renal plasma flow by approximately 65%. However, despite the sodium retention induced by these hemodynamic changes, there were no significant differences in renal hemodynamics or sodium excretion between the two kidneys during pulmonary artery constriction. In contrast, after release of the pulmonary artery occluder on day 9, sodium excretion increased more (approximately 28% during the initial 24 h) in innervated than in denervated kidneys. These results suggest that the renal nerves are relatively unimportant in promoting sodium retention in this model of low cardiac output but contribute significantly to the short-term elimination of sodium after partial restoration of cardiac output and mean arterial pressure.
This article has been cited by other articles:
![]() |
T. E. Lohmeier, J. R. Lohmeier, A. Haque, and D. A. Hildebrandt Baroreflexes prevent neurally induced sodium retention in angiotensin hypertension Am J Physiol Regulatory Integrative Comp Physiol, October 1, 2000; 279(4): R1437 - R1448. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. E. Lohmeier, H. L. Mizelle, G. A. Reinhart, and J.-P. Montani Influence of angiotensin on the early progression of heart failure Am J Physiol Regulatory Integrative Comp Physiol, January 1, 2000; 278(1): R74 - R86. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. E. Lohmeier, D. A. Hildebrandt, and W. A. Hood Renal Nerves Promote Sodium Excretion During Long-Term Increases in Salt Intake Hypertension, January 1, 1999; 33(1): 487 - 492. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. E. Lohmeier, G. A. Reinhart, H. L. Mizelle, M. Han, and M. M. Dean Renal denervation supersensitivity revisited Am J Physiol Regulatory Integrative Comp Physiol, October 1, 1998; 275(4): R1239 - R1246. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |