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Am J Physiol Regul Integr Comp Physiol 285: R1402-R1409, 2003; doi:10.1152/ajpregu.00027.2003
0363-6119/03 $5.00
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NEUROHUMORAL CONTROL OF CIRCULATION AND HYPERTENSION

Mineralocorticoids act centrally to regulate blood-borne tumor necrosis factor-{alpha} in normal rats

Joseph Francis,1 Terry Beltz,2 Alan Kim Johnson,2 and Robert B. Felder1,3

Departments of 1Internal Medicine and 2Psychology, University of Iowa; and 3Veterans Affairs Medical Center, Iowa City, Iowa 52242

Submitted 17 January 2003 ; accepted in final form 13 August 2003

Excessive mineralocorticoid receptor (MR) stimulation induces neurohumoral excitation and cardiac and vascular fibrosis. In heart failure (HF) rats, with excessive neurohumoral drive, central infusion of the MR antagonist spironolactone (SL) decreases blood-borne TNF-{alpha}. This study aimed to determine whether DOCA, a precursor of aldosterone, acts centrally to stimulate TNF-{alpha} production in normal rats. DOCA (5 mg sc daily for 8 days) induced a progressive increase in TNF-{alpha} beginning on day 3 and increased tissue TNF-{alpha} in hypothalamus, pituitary, and heart but not in other brain and peripheral tissues harvested on day 9. A continuous intracerebroventricular infusion of SL (100 ng/h) blocked the plasma TNF-{alpha} response. Oral SL (1 mg/kg) blocked the plasma and tissue TNF-{alpha} responses. Thus DOCA increases TNF-{alpha} in brain, heart, and blood in normal rats. Activation of brain MR appears to account for the increase in plasma TNF-{alpha}. These findings have important implications for the understanding of pathophysiological states (e.g., HF, hypertension) characterized by high circulating levels of aldosterone.

aldosterone; deoxycorticosterone acetate; spironolactone; brain; heart


Address for reprint requests and other correspondence: R. B. Felder, Univ. of Iowa College of Medicine, E318-GH, 200 Hawkins Dr., Iowa City, IA 52242 (E-mail: robert-felder{at}uiowa.edu).




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