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This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: 296/6/R1889    most recent 90931.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Michaels, S. Articles by Evans, R. G. PubMed PubMed Citation Articles by Michaels, S. Articles by Evans, R. G.

WATER AND ELECTROLYTE HOMEOSTASIS

Altered responsiveness of the kidney to activation of the renal nerves in fat-fed rabbits

Departments of ¹Physiology and ²Anatomy and Developmental Biology, Monash University, Melbourne; ³Baker IDI Heart and Diabetes Institute, Melbourne, Australia; ⁴University of North Texas Health Science Center, Fort Worth, Texas; and ⁵Department of Physiology, University of Auckland, New Zealand

Submitted 18 November 2008 ; accepted in final form 22 March 2009

We tested whether mild adiposity alters responsiveness of the kidney to activation of the renal sympathetic nerves. After rabbits were fed a high-fat or control diet for 9 wk, responses to reflex activation of renal sympathetic nerve activity (RSNA) with hypoxia and electrical stimulation of the renal nerves (RNS) were examined under pentobarbital anesthesia. Fat pad mass and body weight were, respectively, 74% and 6% greater in fat-fed rabbits than controls. RNS produced frequency-dependent reductions in renal blood flow, cortical and medullary perfusion, glomerular filtration rate, urine flow, and sodium excretion and increased renal plasma renin activity (PRA) overflow. Responses of sodium excretion and medullary perfusion were significantly enhanced by fat feeding. For example, 1 Hz RNS reduced sodium excretion by 79 ± 4% in fat-fed rabbits and 46 ± 13% in controls. RNS (2 Hz) reduced medullary perfusion by 38 ± 11% in fat-fed rabbits and 9 ± 4% in controls. Hypoxia doubled RSNA, increased renal PRA overflow and medullary perfusion, and reduced urine flow and sodium excretion, without significantly altering mean arterial pressure (MAP) or cortical perfusion. These effects were indistinguishable in fat-fed and control rabbits. Neither MAP nor PRA were significantly greater in conscious fat-fed than control rabbits. These observations suggest that mild excess adiposity can augment the antinatriuretic response to renal nerve activation by RNS, possibly through altered neural control of medullary perfusion. Thus, sodium retention in obesity might be driven not only by increased RSNA, but also by increased responsiveness of the kidney to RSNA.

hypertension; hypoxia; kidney circulation; obesity; kidney medulla; renal sympathetic nerves; renin-angiotensin system; sodium excretion