Document Detail


Effects of non-steroidal anti-inflammatory drugs on prostacyclin and thromboxane biosynthesis in patients with mild essential hypertension.
MedLine Citation:
PMID:  2291866     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
P Minuz; S E Barrow; J R Cockcroft; J M Ritter
Related Documents :
3036496 - The control of hypertension with dibutyryl cyclic amp.
3321806 - Hemodynamic effects of the anti-hypertensive agent ketanserin in hypertension in man.
23212396 - Pressure-diameter relationship in human coronary arteries.
12574096 - Lipid peroxidation is not increased in patients with untreated mild-to-moderate hyperte...
11712776 - Invest substudies: design and patient characteristics.
3501866 - Hemodynamic effects of calcitonin gene-related peptide in conscious rats.
Publication Detail:
Type:  Clinical Trial; Comparative Study; Controlled Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  British journal of clinical pharmacology     Volume:  30     ISSN:  0306-5251     ISO Abbreviation:  Br J Clin Pharmacol     Publication Date:  1990 Oct 
Date Detail:
Created Date:  1991-04-09     Completed Date:  1991-04-09     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  7503323     Medline TA:  Br J Clin Pharmacol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  519-26     Citation Subset:  IM    
Affiliation:
Department of Clinical Pharmacology, Royal Postgraduate Medical School, Hammersmith Hospital, London.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
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:
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

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  D-penicillamine and D-penicillamine-protein disulphide in plasma and synovial fluid of patients with...
Next Document:  Central effects of the angiotensin-converting enzyme inhibitor, captopril. I. Performance and subjec...