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Research Article Free access | 10.1172/JCI109249

Evidence that the Brain Participates in the Humoral Natriuretic Mechanism of Blood Volume Expansion in the Dog

George J. Kaloyanides, Murgurdich B. Balabanian, Ralph L. Bowman, and Philip Pool

Division of Nephrology, University of California at Los Angeles, Sepulveda, California 91343

San Fernando Valley Medical Program and the Veterans Administration Hospital, Sepulveda, California 91343

Find articles by Kaloyanides, G. in: PubMed | Google Scholar

Division of Nephrology, University of California at Los Angeles, Sepulveda, California 91343

San Fernando Valley Medical Program and the Veterans Administration Hospital, Sepulveda, California 91343

Find articles by Balabanian, M. in: PubMed | Google Scholar

Division of Nephrology, University of California at Los Angeles, Sepulveda, California 91343

San Fernando Valley Medical Program and the Veterans Administration Hospital, Sepulveda, California 91343

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

Division of Nephrology, University of California at Los Angeles, Sepulveda, California 91343

San Fernando Valley Medical Program and the Veterans Administration Hospital, Sepulveda, California 91343

Find articles by Pool, P. in: PubMed | Google Scholar

Published December 1, 1978 - More info

Published in Volume 62, Issue 6 on December 1, 1978
J Clin Invest. 1978;62(6):1288–1295. https://doi.org/10.1172/JCI109249.
© 1978 The American Society for Clinical Investigation
Published December 1, 1978 - Version history
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Abstract

We examined the role of the central nervous system in the activation of the humoral natriuretic mechanism elicited by blood volume expansion. Studies were performed in anesthetized dogs pretreated with deoxycorticosterone acetate (15 mg/day) and sodium chloride for 12 days. An isolated dog kidney perfused with blood from the femoral artery of the volume expanded dog served as the bioassay system for the humoral natriuretic factor. In group I volume expansion of intact dogs (n = 14) with equilibrated blood promoted an increase in fractional sodium excretion (FENa) from a control level of 2.6±0.5 to 13.6±1.6%, P <0.001. In the isolated kidney FENa increased from 3.6±0.8 to 6.8±1.1%, P <0.01. The natriuresis from the isolated kidney occurred in the absence of significant changes in renal arterial pressure, glomerular filtration rate, plasma protein concentration, or packed cell volume, whereas renal blood flow decreased slightly. In group II (n = 20) the dogs were decapitated by means of a specially designed neck vise. In 10 dogs blood pressure was supported by a constant infusion of dopamine (3.8±0.7 μg/min per kg body weight). Despite the fact that in response to the same volume stimulus, decapitated dogs manifested an increase in blood volume and cardiac output similar in magnitude to that of intact dogs whereas the rise in mean arterial pressure of decapitated dogs exceeded that of intact dogs, the natriuretic response of decapitated dogs was significantly less than that of intact dogs. FENa in decapitated dogs increased 4.7±1.1 compared to 11.1±1.4% in intact dogs (p <0.01). Furthermore, volume expansion of decapitated dogs failed to elicit a natriuretic response from the isolated kidney. FENa in the isolated kidney measured 2.6±0.4 before and 2.6±0.4% after blood volume expansion. These data indicate that decapitation inhibits activation of the humoral natriuretic mechanism elicited by blood volume expansion and are consistent with the interpretation that the brain is the source of the natriuretic factor or that the brain participates in the activation of the humoral natriuretic mechanism at some other site in the body.

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