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Sympathectomy does not inhibit dexamethasone‐induced hypertension
Author(s) -
SotoPina Alexandra Estela,
Kadapakkam Sheela,
Mehring Cynthia,
HinojosaLaborde Carmen,
Strong Randy
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.594.4
Subject(s) - sympathectomy , medicine , dexamethasone , adrenal medulla , tyrosine hydroxylase , endocrinology , blood pressure , mean arterial pressure , heart rate , catecholamine , glucocorticoid , sympathetic nervous system , dopamine
Dexamethasone (DEX) induces hypertension and increases the expression of tyrosine hydroxylase, the rate limiting step in catecholamine synthesis in the adrenal medulla. We have shown that DEX increases mean arterial pressure (MAP, 119 ± 0.9 mm Hg), and surgical removal of the adrenal medulla does not attenuate this response (120.4 ± 1.3 mm Hg). Our hypothesis is that DEX induces hypertension by systemic sympathetic activation. The purpose of this study was to determine the effect of sympathetic nerve ablation on DEX‐induced hypertension. Fischer 344 rats were implanted with radio‐telemetry transmitters to record MAP and heart rate (HR). After baseline recording, rats underwent chemical sympathectomy with 6‐hydroxydopamine (6‐OHDA, 20 mg/kg, i.p. for 3 days). 6‐OHDA reduced MAP by 7.2 ± 1.0 mmHg, and increased HR by 55±17 bpm. Subsequent treatment with DEX (0.1 mg/day for 7 days) elevated MAP by 12.2 ± 1.6 mmHg and reduced HR by 18±7 bpm. Similar to adrenalmedullectomy, 6‐OHDA did not abolish the hypertensive effects of DEX chronic treatment. This study will provide an insight about the role of the adrenal medulla and peripheral sympathectomy in glucocorticoid‐induced hypertension. Support provided by: Department of Veterans Affairs.