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2-adrenoceptors in caudal
ventrolateral medulla to cardiovascular regulation in rat
Third Department of Internal Medicine, University of The Ryukyus School of Medicine, Nishihara, Okinawa 903-01, Japan
The inhibitory action of
2-agonists on the
cardiovascular neurons has been elucidated in the rostral ventrolateral
medulla (RVLM) but not in the caudal ventrolateral medulla (CVLM). Our study aimed to clarify whether microinjection of clonidine into the
CVLM elicits any cardiovascular effect and whether endogenous
2-adrenoceptor-mediated
mechanisms contribute to the tonic activity of the CVLM neurons. In
male Sprague-Dawley rats (7-9 wk old, 270-320 g) anesthetized
with urethan, unilateral microinjection of 8 nmol of clonidine into the
CVLM (n = 10) increased mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) by 12.1 ± 1.8 mmHg (mean ± SE, P < 0.01) and
25.8 ± 4.8% (P < 0.01), while
heart rate (HR) remained unaltered. Unilateral microinjection of 2 nmol
of SKF-86466, a selective blocker of the
2-adrenoceptors, into the CVLM
(n = 10) decreased MAP, HR, and RSNA
(
11.6 ± 2.6 mmHg,
26 ± 7 beats/min, and
15.3 ± 1.7%, respectively, P < 0.01 for each). Artificial cerebrospinal fluid caused neither a
cardiovascular effect nor a sympathetic response. Prior injection of
SKF-86466 into the ipsilateral CVLM attenuated the effects of
clonidine. Bilateral microinjection of muscimol into the RVLM abolished
the effects of both clonidine and SKF-86466 injected into the CVLM. The
pressor and sympathoexcitatory effects of clonidine injected into the
CVLM suggest a neuroinhibitory action of the drug on the CVLM neurons.
In addition,the depressor and sympathoinhibitory effects of SKF-86466
injected into the CVLM indicated that activation of
2-adrenoceptors by endogenous
ligand inhibits CVLM neurons. The effects of clonidine and the
2-adrenoceptor antagonist in the CVLM require the integrity of the RVLM.
imidazole receptor; clonidine; blood pressure; renal sympathetic nerve activity
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