| Modulation of tissue responsiveness to angiotensin-II in hyperprolactinemic subjects. | |
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MedLine Citation:
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PMID: 2370301 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The present studies were designed to test the hypothesis that hyperprolactinemia modulates target tissue responsiveness to angiotensin-II (AII). Adrenal and pressor responses to AII infusions were determined in six patients with PRL-secreting pituitary microadenomas and in five normal controls during defined electrolyte balance. Hyperprolactinemic and normal subjects had similar mean blood pressures while on a regular Na intake (82.5 +/- 0.5 vs. 81.2 +/- 0.3 mm Hg). However, after 4 days of Na loading (200 meq/day), the mean blood pressure in hyperprolactinemic subjects was higher than that in normal (86.6 +/- 1 vs. 83.4 +/- 0.8 mm Hg; P less than 0.05). In addition, enhancement of the mean blood pressure response to three doses of AII was noted in hyperprolactinemic subjects (P less than 0.05) compared to that in normal subjects. After 4 days of Na restriction (10 meq/day), the mean blood pressure in hyperprolactinemic subjects was similar to that in normal subjects (79.7 +/- 0.6 vs. 78.9 +/- 1 mm Hg). However, despite adequate Na restriction, the pressor response to AII continued to be enhanced (P less than 0.05) in hyperprolactinemic subjects. There were no differences in plasma or urinary electrolytes or in PRA between hyperprolactinemic and normal subjects. Hyperprolactinemic subjects had higher basal (P less than 0.01), AII-stimulated (P less than 0.05), and ACTH-stimulated (P less than 0.02) aldosterone levels during Na loading, but not during Na restriction. The differences disappeared after the correction of the hyperprolactinemia. The data demonstrate significant alterations in adrenal and pressor responsiveness in hyperprolactinemic subjects and suggest a modulating role for PRL on vascular reactivity and steroid biosynthesis. The precise mechanism has not been determined, but may be secondary to PRL-induced up-regulation of adrenal and vascular AII receptors. |
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Authors:
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B M Arafah; N H Gordon; R Salazar; J G Douglas |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: The Journal of clinical endocrinology and metabolism Volume: 71 ISSN: 0021-972X ISO Abbreviation: J. Clin. Endocrinol. Metab. Publication Date: 1990 Jul |
Date Detail:
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Created Date: 1990-08-23 Completed Date: 1990-08-23 Revised Date: 2007-11-14 |
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: 60-6 Citation Subset: AIM; IM |
Affiliation:
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Division of Hypertension and Endocrinology, University Hospitals of Cleveland, Ohio 44106. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adenoma
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secretion Adrenal Glands / drug effects*, metabolism Adult Angiotensin II / pharmacology* Blood Pressure / drug effects Female Humans Hyperprolactinemia / metabolism* Infusions, Intravenous Male Pituitary Neoplasms / secretion Potassium / metabolism Prolactin / secretion* Sodium / metabolism Steroids / biosynthesis Water-Electrolyte Balance / drug effects, physiology |
| Grant Support | |
ID/Acronym/Agency:
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HL-22990/HL/NHLBI NIH HHS; HL-39012/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Steroids; 11128-99-7/Angiotensin II; 7440-09-7/Potassium; 7440-23-5/Sodium; 9002-62-4/Prolactin |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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