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-adrenergic mechanism
Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan 48201
Previously, we have shown that
activation of adenosine A2a receptors in the subpostremal
nucleus tractus solitarii (NTS) via microinjection of the selective
A2a receptor agonist CGS-21680 elicits potent,
dose-dependent decreases in mean arterial pressure and preferential,
marked hindlimb vasodilation. Although A2a receptor activation does not change lumbar sympathetic nerve activity, it does
markedly enhance the preganglionic adrenal sympathetic nerve activity,
which will increase epinephrine release and could subsequently elicit
hindlimb vasodilation via activation of
2-adrenergic receptors. Therefore we investigated whether this hindlimb vasodilation was due to neural or humoral mechanisms. In
chloralose-urethan-anesthetized male Sprague-Dawley rats, we monitored
cardiovascular responses to stimulation of NTS adenosine
A2a receptors (CGS-21680, 20 pmol/50 nl) in the intact
control animals; after pretreatment with propranolol (2 mg/kg iv), a
-adrenergic antagonist; after bilateral lumbar sympathectomy; after
bilateral adrenalectomy; and after combined bilateral lumbar
sympathectomy and adrenalectomy. After
-adrenergic blockade,
stimulation of NTS adenosine A2a receptors produced a
pressor response and a hindlimb vasoconstriction. Lumbar sympathectomy reduced the vasodilation seen in the intact animals by ~40%, and adrenalectomy reduced it by ~80%. The combined sympathectomy and adrenalectomy virtually abolished the hindlimb vasodilation evoked by
NTS A2a receptor activation. We conclude that the
preferential, marked hindlimb vasodilation produced by stimulation of
NTS adenosine A2a receptors is mediated by both the
efferent sympathetic nerves directed to the hindlimb and the adrenal
glands via primarily a
-adrenergic mechanism.
adrenal gland; sympathetic nervous system; epinephrine; adenosine; purines; nucleus tractus solitarii
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