| Effects of non-steroidal anti-inflammatory drugs on prostacyclin and thromboxane biosynthesis in patients with mild essential hypertension. | |
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MedLine Citation:
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PMID: 2291866 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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1. The effects of non-steroidal anti-inflammatory drugs (NSAID) on prostacyclin and thromboxane biosynthesis and on blood pressure were determined in 46 patients with mild essential hypertension. Patients who had abstained from antihypertensive therapy for 2 weeks before study were treated with either aspirin, ibuprofen, sulindac or placebo for 7 days. 2. Excretion rates of 2,3-dinor-6-oxo-prostaglandin (PG) F1 alpha, 6-oxo-PGF1 alpha, 2,3-dinorthromboxane (TX) B2 and TXB2 were measured as indices of prostacyclin and TXA2 biosynthesis. Samples were assayed using immunoaffinity chromatography and gas chromatography/electron capture chemical ionisation mass spectrometry. 3. Aspirin and ibuprofen reduced urinary excretion of all prostacyclin- and thromboxane-derived products. Sulindac inhibited excretion of 2,3-dinor-6-oxo-PGF1 alpha, 6-oxo-PGF1 alpha and 2,3-dinor-TXB2, but had no significant effect on TXB2. 4. Systolic blood pressure increased in the ibuprofen-treated group when compared with the placebo group. There were no other significant changes in systolic or diastolic pressure in any of the treatment groups. Among the patients as a whole, there was a significant negative correlation between change in blood pressure and change in excretion of the prostacyclin-derived but not of the thromboxane-derived products. 5. We conclude that, in patients with mild essential hypertension, neither sulindac nor aspirin (in the doses used) selectively spares prostacyclin biosynthesis by the kidney. The significant relationship between increase in blood pressure and reduction in prostacyclin biosynthesis favours the possibility that in individuals who become hypertensive, prostacyclin biosynthesis determines, in part, the severity of the hypertensive state. |
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Authors:
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P Minuz; S E Barrow; J R Cockcroft; J M Ritter |
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Publication Detail:
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Type: Clinical Trial; Comparative Study; Controlled Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: British journal of clinical pharmacology Volume: 30 ISSN: 0306-5251 ISO Abbreviation: Br J Clin Pharmacol Publication Date: 1990 Oct |
Date Detail:
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Created Date: 1991-04-09 Completed Date: 1991-04-09 Revised Date: 2009-11-18 |
Medline Journal Info:
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Nlm Unique ID: 7503323 Medline TA: Br J Clin Pharmacol Country: ENGLAND |
Other Details:
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Languages: eng Pagination: 519-26 Citation Subset: IM |
Affiliation:
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Department of Clinical Pharmacology, Royal Postgraduate Medical School, Hammersmith Hospital, London. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adult Aged Anti-Inflammatory Agents, Non-Steroidal / pharmacology* Aspirin / pharmacology Blood Pressure / drug effects Chromatography, Affinity Epoprostenol / biosynthesis*, blood Female Gas Chromatography-Mass Spectrometry Humans Hypertension / metabolism*, physiopathology Ibuprofen / pharmacology Kidney / metabolism Male Middle Aged Sulindac / pharmacology Thromboxanes / biosynthesis*, blood |
| Chemical | |
Reg. No./Substance:
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0/Anti-Inflammatory Agents, Non-Steroidal; 0/Thromboxanes; 15687-27-1/Ibuprofen; 35121-78-9/Epoprostenol; 38194-50-2/Sulindac; 50-78-2/Aspirin |
| Comments/Corrections | |
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