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Research Article Free access | 10.1172/JCI107895

Mechanism of Effect of Thoracic Inferior Vena Cava Constriction on Renal Water Excretion

Robert J. Anderson, Pravit Cadnapaphornchai, Judith A. Harbottle, Keith M. McDonald, and Robert W. Schrier

Department of Medicine, University of Colorado Medical Center, Denver, Colorado 80220

Find articles by Anderson, R. in: PubMed | Google Scholar

Department of Medicine, University of Colorado Medical Center, Denver, Colorado 80220

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Department of Medicine, University of Colorado Medical Center, Denver, Colorado 80220

Find articles by Harbottle, J. in: PubMed | Google Scholar

Department of Medicine, University of Colorado Medical Center, Denver, Colorado 80220

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Department of Medicine, University of Colorado Medical Center, Denver, Colorado 80220

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Published December 1, 1974 - More info

Published in Volume 54, Issue 6 on December 1, 1974
J Clin Invest. 1974;54(6):1473–1479. https://doi.org/10.1172/JCI107895.
© 1974 The American Society for Clinical Investigation
Published December 1, 1974 - Version history
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Abstract

Persistent secretion of vasopressin and/ or diminished distal fluid delivery have been proposed to explain the impaired water excretion associated with low-output cardiac failure. In the present investigation cardiac output (CO) was diminished in anesthetized dogs undergoing a water diuresis by constriction of the thoracic inferior vena cava (TIVC). In intact animals (group I) acute TIVC constriction decreased CO from 3.5 to 2.2 liters/min (P < 0.005) as urinary osmolality (Uosm) increased from 103 to 543 mosmols/ kg (P < 0.001) and free water clearance (CH2o) decreased from 2.1 to -0.6 ml/min (P < 0.001). This antidiuretic effect was disassociated from changes in renal arterial and venous pressures, glomerular filtration rate, solute excretion, and renal innervation. To examine the role of vasopressin in this antidiuresis, studies (group II) were performed in acutely hypophysectomized, steroid-replaced animals. In these animals TIVC constriction decreased CO to a similar degree from 3.4 to 2.1 liters/min (P < 0.001). However, the effects on Uosm (87-104 mosmols/kg) and CH2o (2.1-1.6 ml/min) were significantly less than in intact dogs. In another group of hypophysectomized animals, (group III) renal arterial and venous pressures were not controlled, and the effect of TIVC constriction on Uosm was not significant (65-79 mosmols/kg) although CH2o decreased from 3.3 to 1.9 ml/min (P < 0.001). In both the group II and III studies, there were linear correlations between the changes in CH2o and the urine flow. Studies were also performed in baroreceptor-denervated animals with intact hypothalamo-neurohypophyseal tracts, and acute TIVC constriction altered neither Uosm nor CH2o when renal arterial pressure was controlled. These results therefore indicate that the effect of TIVC constriction on Uosm is primarily vasopressin mediated while the effect on CH2o is mediated both by vasopressin release and diminished distal fluid delivery. A decrease in renal arterial pressure, or some consequence thereof, seems to be an important determinant of the latter effect.

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