| The role of thyroid hormone in blood pressure homeostasis: evidence from short-term hypothyroidism in humans. | |
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MedLine Citation:
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PMID: 11994331 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Arterial hypertension is known to be frequently associated with thyroid dysfunction, with a particularly high prevalence in chronic hypothyroidism. However, to our knowledge no comprehensive study addressed causal mechanisms possibly involved in this association. We here report the physiological relationships between blood pressure and neuro-humoral modifications induced by acute hypothyroidism in normotensive subjects. Twelve normotensive patients with previous total thyroidectomy were studied. Ambulatory 24-h blood pressure monitoring was performed, and free T(3), free T(4), TSH, PRA, aldosterone, cortisol, adrenaline, and noradrenaline were assayed 6 wk after oral L-T(4) withdrawal (phase 1) and 2 months after resumption of treatment (phase 2). During the hypothyroid state (TSH, 68.1 +/- 27.7 microIU/ml; mean +/- SD), daytime arterial systolic levels slightly, but significantly, increased (125.5 +/- 9.7 vs. 120.4 +/- 10.8 mm Hg; P < 0.05), and daytime diastolic levels (84.6 +/- 7.9 vs. 76.4 +/- 6.8 mm Hg; P < 0.001), noradrenaline (2954 +/- 1578 vs. 1574 +/- 962 pmol/liter; P < 0.001), and adrenaline (228.4 +/- 160 vs. 111.3 +/- 46.1 pmol/liter; P < 0.05) also increased. PRA remained unchanged (0.49 +/- 0.37 vs. 0.35 +/- 0.21 ng/ml.h; P = NS), whereas both aldosterone (310.3 +/- 151 vs. 156.9 +/- 67.5 pmol/liter; P < 0.005) and cortisol (409.2 +/- 239 vs. 250.9 +/- 113 pmol/liter; P < 0.02) significantly increased. By using univariate logistic regression daytime arterial diastolic values, noradrenaline and aldosterone were found to be significantly related to the hypothyroid state (P < 0.02, P < 0.036, and P < 0.024, respectively). In conclusion, our data show that thyroid hormones participate in the control of systemic arterial blood pressure homeostasis in normotensive subjects. The observed sympathetic and adrenal activation in hypothyroidism, which is reversible with thyroid hormone treatment, may also contribute to the development of arterial hypertension in human hypothyroidism. |
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Authors:
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Enza Fommei; Giorgio Iervasi |
Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: The Journal of clinical endocrinology and metabolism Volume: 87 ISSN: 0021-972X ISO Abbreviation: J. Clin. Endocrinol. Metab. Publication Date: 2002 May |
Date Detail:
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Created Date: 2002-05-07 Completed Date: 2002-06-14 Revised Date: 2004-11-17 |
Medline Journal Info:
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Nlm Unique ID: 0375362 Medline TA: J Clin Endocrinol Metab Country: United States |
Other Details:
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Languages: eng Pagination: 1996-2000 Citation Subset: AIM; IM |
Affiliation:
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National Council of Research, University of Pisa, Italy. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adrenal Glands
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physiopathology Adult Aged Aldosterone / blood Blood Pressure / physiology* Combined Modality Therapy Cortisone / blood Female Homeostasis / physiology* Humans Hypothyroidism / etiology, physiopathology* Male Middle Aged Regression Analysis Renin / blood Sympathetic Nervous System / physiopathology Thyroid Hormones / physiology* Thyroid Neoplasms / radiotherapy, surgery Thyroidectomy / adverse effects |
| Chemical | |
Reg. No./Substance:
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0/Thyroid Hormones; 52-39-1/Aldosterone; 53-06-5/Cortisone; EC 3.4.23.15/Renin |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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