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Activation of {alpha}2-receptors in the rostral ventrolateral medulla evokes natriuresis by a renal nerve mechanism
1 Department of Physiological Sciences, Medical Center Federal University of Espirito Santo, Vitoria, Brazil 29040 - 090; and 2 Department of Pharmacology and Experimental Therapeutics, Louisiana State University Health Sciences Center, New Orleans, Louisiana 70112 The contribution of 2 -receptor...
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Published in: | American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 2001-07, Vol.281 (1), p.98 |
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Main Authors: | , , , |
Format: | Article |
Language: | English |
Online Access: | Get full text |
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Summary: | 1 Department of Physiological Sciences, Medical Center
Federal University of Espirito Santo, Vitoria, Brazil
29040 - 090; and 2 Department of Pharmacology and
Experimental Therapeutics, Louisiana State University Health Sciences
Center, New Orleans, Louisiana 70112
The
contribution of 2 -receptor mechanisms in the rostral
ventrolateral medulla (RVLM) in mediating the enhanced renal excretory responses evoked by the intravenous infusion of the
2 -receptor agonist xylazine was examined in
ketamine-anesthetized rats. In ketamine-anesthetized rats, the
bilateral microinjection of the 2 -receptor antagonist
yohimbine into the RVLM significantly reduced the enhanced levels of
urine flow rate (V) and urinary sodium excretion (UNaV) produced by
xylazine. In contrast, microinjection of yohimbine into the RVLM of
chronically bilaterally renal-denervated rats significantly reduced the
xylazine-evoked diuretic, but not natriuretic, response. In separate
ketamine-anesthetized rats, intravenous xylazine infusion produced a
near complete inhibition of renal sympathetic nerve activity (RSNA).
The subsequent microinjection of yohimbine into the RVLM reversed this
neural response and concurrently decreased V and UNaV. Together, these
results indicate that during intravenous infusion, xylazine activates
2 -receptor mechanisms in the RVLM to selectively promote
urinary sodium excretion by a renal nerve-dependent pathway. In
contrast, activation of 2 -receptor in the RVLM affects
the renal handling of water by a pathway independent of the renal
nerves. This latter pathway may involve an interaction with other brain
regions involved in antidiuretic hormone release (e.g., paraventricular
nucleus of the hypothalamus).
renal sympathetic nerves; renal excretory function; urine flow
rate; urinary sodium excretion; central nervous system; microinjection |
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ISSN: | 0363-6119 1522-1490 |