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Research ArticleCardiovascular

A Novel Model of Dexamethasone-Induced Hypertension: Use in Investigating the Role of Tyrosine Hydroxylase

Alexandra E. Soto-Piña, Cynthia Franklin, C.S. Sheela Rani, Helmut Gottlieb, Carmen Hinojosa-Laborde and Randy Strong
Journal of Pharmacology and Experimental Therapeutics September 2016, 358 (3) 528-536; DOI: https://doi.org/10.1124/jpet.116.234005
Alexandra E. Soto-Piña
Universidad Autónoma del Estado de México, Facultad de Medicina, Toluca, México (A.E.S.-P.); Department of Pharmacology, University of Texas Health Science Center at San Antonio, San Antonio, Texas (C.S.S.R., C.H.-L., R.S.); Feik School of Pharmacy, University of the Incarnate Word, San Antonio, Texas (H.G., C.F.); and Audie L. Murphy Division, South Texas Veterans Health Care System, San Antonio, Texas (R.S.)
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Cynthia Franklin
Universidad Autónoma del Estado de México, Facultad de Medicina, Toluca, México (A.E.S.-P.); Department of Pharmacology, University of Texas Health Science Center at San Antonio, San Antonio, Texas (C.S.S.R., C.H.-L., R.S.); Feik School of Pharmacy, University of the Incarnate Word, San Antonio, Texas (H.G., C.F.); and Audie L. Murphy Division, South Texas Veterans Health Care System, San Antonio, Texas (R.S.)
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C.S. Sheela Rani
Universidad Autónoma del Estado de México, Facultad de Medicina, Toluca, México (A.E.S.-P.); Department of Pharmacology, University of Texas Health Science Center at San Antonio, San Antonio, Texas (C.S.S.R., C.H.-L., R.S.); Feik School of Pharmacy, University of the Incarnate Word, San Antonio, Texas (H.G., C.F.); and Audie L. Murphy Division, South Texas Veterans Health Care System, San Antonio, Texas (R.S.)
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Helmut Gottlieb
Universidad Autónoma del Estado de México, Facultad de Medicina, Toluca, México (A.E.S.-P.); Department of Pharmacology, University of Texas Health Science Center at San Antonio, San Antonio, Texas (C.S.S.R., C.H.-L., R.S.); Feik School of Pharmacy, University of the Incarnate Word, San Antonio, Texas (H.G., C.F.); and Audie L. Murphy Division, South Texas Veterans Health Care System, San Antonio, Texas (R.S.)
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Carmen Hinojosa-Laborde
Universidad Autónoma del Estado de México, Facultad de Medicina, Toluca, México (A.E.S.-P.); Department of Pharmacology, University of Texas Health Science Center at San Antonio, San Antonio, Texas (C.S.S.R., C.H.-L., R.S.); Feik School of Pharmacy, University of the Incarnate Word, San Antonio, Texas (H.G., C.F.); and Audie L. Murphy Division, South Texas Veterans Health Care System, San Antonio, Texas (R.S.)
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Randy Strong
Universidad Autónoma del Estado de México, Facultad de Medicina, Toluca, México (A.E.S.-P.); Department of Pharmacology, University of Texas Health Science Center at San Antonio, San Antonio, Texas (C.S.S.R., C.H.-L., R.S.); Feik School of Pharmacy, University of the Incarnate Word, San Antonio, Texas (H.G., C.F.); and Audie L. Murphy Division, South Texas Veterans Health Care System, San Antonio, Texas (R.S.)
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Abstract

Our objective was to study hypertension induced by chronic administration of synthetic glucocorticoid, dexamethasone (DEX), under nonstressful conditions and examine the role of catecholamine biosynthesis. To achieve this, we did the following: 1) used radiotelemetry to record mean arterial pressure (MAP) and heart rate (HR) in freely moving rats, and 2) administered different doses of DEX in drinking water. To evaluate the involvement of tyrosine hydroxylase (TH), the rate-limiting step in catecholamine biosynthesis, we treated rats with the TH inhibitor, α-methyl-para-tyrosine (α-MPT), for 3 days prior to administration of DEX and assessed TH mRNA and protein expression by quantitative real-time polymerase chain reaction and Western blot in the adrenal medulla. We observed a dose-dependent elevation in blood pressure with a DEX dose of 0.3 mg/kg administered for 10 days, significantly increasing MAP by +15.0 ± 1.1 mm Hg, while concomitantly reducing HR. Although this DEX treatment also significantly decreased body weight, pair-fed animals that showed similar decreases in body weight due to lowered food intake were not hypertensive, suggesting that body weight changes may not account for DEX-induced hypertension. Chronic DEX treatment significantly increased the TH mRNA and protein levels in the adrenal medulla, and α-MPT administration not only reduced DEX pressor effects, but also inhibited TH (serine40) phosphorylation. Our study thus validates a novel model to study hypertension induced by chronic intake of DEX in freely moving rats not subject to the confounding factors of previous models and establishes its dependence on concomitant activation of peripheral catecholamine biosynthesis.

Footnotes

    • Received March 28, 2016.
    • Accepted July 8, 2016.
  • This work was supported by the Department of Veteran Affairs (to R.S.), Consejo Nacional de Ciencia y Technología (to A.E.S.-P.), and a predoctoral award from the American Heart Association (to A.E.S.-P.).

  • dx.doi.org/10.1124/jpet.116.234005.

  • Copyright © 2016 by The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 358 (3)
Journal of Pharmacology and Experimental Therapeutics
Vol. 358, Issue 3
1 Sep 2016
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Research ArticleCardiovascular

A Novel Model of Dexamethasone-Induced Hypertension

Alexandra E. Soto-Piña, Cynthia Franklin, C.S. Sheela Rani, Helmut Gottlieb, Carmen Hinojosa-Laborde and Randy Strong
Journal of Pharmacology and Experimental Therapeutics September 1, 2016, 358 (3) 528-536; DOI: https://doi.org/10.1124/jpet.116.234005

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Research ArticleCardiovascular

A Novel Model of Dexamethasone-Induced Hypertension

Alexandra E. Soto-Piña, Cynthia Franklin, C.S. Sheela Rani, Helmut Gottlieb, Carmen Hinojosa-Laborde and Randy Strong
Journal of Pharmacology and Experimental Therapeutics September 1, 2016, 358 (3) 528-536; DOI: https://doi.org/10.1124/jpet.116.234005
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