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AJP - Regulatory, Integrative and Comparative Physiology, Vol 255, Issue 1 6-13, Copyright © 1988 by American Physiological Society
ARTICLES |
H. D. Schultz, D. G. Gardner, C. F. Deschepper, H. M. Coleridge and J. C. Coleridge
Department of Medicine, University of California, San Francisco 94143-0130.
Administration of atrial natriuretic factor (ANF) to anesthetized rats decreases renal nerve activity (RNA), an effect prevented by vagotomy but not by atropine. We sought to determine whether afferent vagal C-fibers mediate the inhibition of sympathetic outflow. ANF (2.5 micrograms/kg iv) decreased mean arterial pressure (MAP) by 25 +/- 2 mmHg, RNA by 11 +/- 5%, and least splanchnic nerve activity (LSNA) by 10 +/- 4% in anesthetized rats with arterial baroreceptors intact, and by 40 +/- 3 mmHg, 28 +/- 7%, and 23 +/- 4%, respectively, in sinoaortic-denervated rats. Inhibition of RNA and LSNA by ANF was reduced slightly by cooling the vagi to 6 or 7 degrees C, a temperature at which conduction in A-fibers was blocked and that in C-fibers attenuated; inhibition was abolished when C-fibers were blocked by cooling to 0 degrees C. We conclude that the inhibition of RNA and LSNA by ANF was mediated by afferent vagal C-fibers. We also obtained evidence that the aortic nerves contribute to ANF-induced inhibition of RNA. Our results support the notion that ANF evokes a generalized decrease in sympathetic tone that contributes to the hypotension, cardiac inhibition, and natriuresis accompanying systemic administration of the peptide.
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