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Role of adrenal medulla in dexamethasone‐induced hypertension
Author(s) -
SotoPina Alexandra Estela,
Kadapakkam Sheela,
Mehring Cynthia,
HinojosaLaborde Carmen,
Strong Randy
Publication year - 2009
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.23.1_supplement.969.14
Subject(s) - adrenal medulla , dexamethasone , endocrinology , medicine , blood pressure , tyrosine hydroxylase , catecholamine , dopamine
Dexamethasone (DEX) was reported to induce hypertension and increase expression of tyrosine hydroxylase (TH), the rate limiting enzymatic step in catecholamine synthesis, in the adrenal medulla. We hypothesized that: 1) DEX increases TH message in the adrenal medulla, and 2) removal of the adrenal medulla attenuates DEX‐induced hypertension. Fisher 344 rats were implanted with radio telemetry transmitters to record blood pressure and heart rate. After 5 days of baseline recording, rats were divided into 2 groups: SHAM and Adrenal medullectomy (ADMX) surgeries. Both groups received vehicle (VEH) or DEX in drinking water (0.1 mg/day for 7 days), starting 5 days after surgery. Adrenal medullas were collected from the SHAM‐VEH and SHAM‐DEX groups and RNA was isolated to quantify TH mRNA by qPCR. The results showed that TH message in DEX treated adrenal medullas increased by 5 fold. DEX increased blood pressure in SHAM‐DEX by 17± 2 mmHg and in ADMX‐DEX by 18±1 mmHg. The results of the study showed that DEX increased TH message in the adrenal medulla, but DEX‐induced hypertension was not prevented by ADMX. We conclude that DEX‐induced hypertension is not completely dependent on the adrenal medulla. Future studies will focus on the contribution of other sympathetic ganglia to DEX‐induced hypertension. Support provided by: Department of Veterans Affairs and CONACYT.
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