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Publication : Alpha2A-adrenergic receptors mediate sympathoinhibitory responses to atrial natriuretic peptide in the mouse anterior hypothalamic nucleus.

First Author  Peng N Year  2003
Journal  Hypertension Volume  41
Issue  3 Pages  571-5
PubMed ID  12623961 Mgi Jnum  J:131890
Mgi Id  MGI:3774788 Doi  10.1161/01.HYP.0000056998.83031.22
Citation  Peng N, et al. (2003) Alpha2A-adrenergic receptors mediate sympathoinhibitory responses to atrial natriuretic peptide in the mouse anterior hypothalamic nucleus. Hypertension 41(3):571-5
abstractText  In the rat, activation of alpha2-adrenergic receptors in the anterior hypothalamic nucleus inhibits sympathetic nervous system activity. Furthermore, local release of atrial natriuretic peptide inhibits norepinephrine release in this nucleus, blocking local activation of alpha2-adrenergic receptors, and thereby contributes to NaCl-sensitive hypertension in spontaneously hypertensive rats. To further test the specificity of this mechanism, either alpha2-adrenergic receptor agonists or atrial natriuretic peptide was microinjected into anterior hypothalamic nucleus of conscious C57BL/6 mice in which the alpha2-adrenergic receptor was functionally deleted by a single point mutation (n=10 per group). In control mice, microinjection of either clonidine or guanabenz (10-3 to 10-7 mol/L) caused a rapid fall in mean arterial pressure that lasted for several minutes. In the knockout mice there was no response to the injection of either dose of either agonist. Microinjection of atrial natriuretic peptide (10-6 to 10-7 mol/L) caused a rapid increase in mean arterial pressure (8.2+/-1.3 and 6.55+/-1.2 mm Hg, respectively) in the control mice that was similar to the responses previously observed in Wistar-Kyoto rats. In contrast, the microinjections did not significantly alter mean arterial pressure in the knockout mice. These experiments demonstrate that in the anterior hypothalamic nucleus of the mouse (and probably in the rat) alpha2A-adrenergic receptors mediate both sympathoinhibitory responses to alpha2-adrenergic receptor agonists and the action of atrial natriuretic peptide.
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