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in rat: the role of central prostaglandins
1 Department of Internal Medicine, University of Iowa, Roy J. and Lucille A. Carver College of Medicine and Medical Service, 2 Veterans Administration Medical Center, Iowa City, Iowa 52242
In pathophysiological conditions,
increased blood-borne TNF-
induces a broad range of biological
effects, including activation of the hypothalamic-pituitary-adrenal
axis and sympathetic drive. In urethane-anesthetized adult
Sprague-Dawley rats, we examined the mechanisms by which blood-borne
TNF- activates neurons in paraventricular nucleus (PVN) of
hypothalamus and rostral ventrolateral medulla (RVLM), two critical
brain regions regulating sympathetic drive in normal and
pathophysiological conditions. TNF- (0.5 µg/kg), administered
intravenously or into ipsilateral carotid artery (ICA), activated PVN
and RLVM neurons and increased sympathetic nerve activity, arterial
pressure, and heart rate. Responses to intravenous TNF- were not
affected by vagotomy but were reduced by mid-collicular decerebration.
Responses to ICA TNF- were substantially reduced by injection of the
cyclooxygenase inhibitor ketorolac (150 µg) into lateral ventricle.
Injection of PGE2 (50 ng) into lateral ventricle or
directly into PVN increased PVN or RVLM activity, respectively, and
sympathetic drive, with shorter onset latency than blood-borne TNF-.
These findings suggest that blood-borne cytokines stimulate
cardiovascular and renal sympathetic responses via a
prostaglandin-dependent mechanism operating at the hypothalamic level.
cytokines; paraventricular nucleus of hypothalamus; rostral ventrolateral medulla; renal sympathetic nerve activity; prostaglandin E2
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