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METABOLITES OF ARACHIDONIC ACID FORMED BY HUMAN GASTROINTESTINAL TISSUES AND THEIR ACTIONS ON THE MUSCLE LAYERS
Author(s) -
BENNETT A.,
HENSBY C.N.,
SANGER G.J.,
STAMFORD I.F.
Publication year - 1981
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1981.tb09989.x
Subject(s) - prostaglandin , ileum , medicine , arachidonic acid , endocrinology , stomach , chemistry , alpha (finance) , thromboxane a2 , muscle contraction , gastrointestinal tract , acetylcholine , peristalsis , prostaglandin d2 , biology , biochemistry , receptor , surgery , enzyme , construct validity , patient satisfaction
1 Gas chromatography‐mass spectrometry demonstrated the presence of arachidonic acid (AA), 6‐keto‐prostaglandin F 1α and thromboxane B 2 (TxB 2 ) in all extracts of homogenized muscle or mucosa from human stomach, terminal ileum or sigmoid colon. Prostaglandin D 2 (PGD 2 ), PGE 2 or PGF 2α were usually found more often in the mucosal extracts. The 12‐hydroxy‐derivative of AA (12‐HETE) was detected in all extracts of the colon but in only some of the other tissues 2 Most prostanoids tested contracted the longitudinal muscle, the order of potency being U‐46619 (an epoxymethano analogue of PGH 2 )>PGE 2 >PGF 2α >PGD 2 ; PGI 2 usually caused relaxation, whereas its breakdown products or TxB 2 had weak and variable effects 3 U‐46619 or, less potently, PGF 2α contracted the circular muscle, whereas PGI 2 and usually PGE 2 caused relaxation. PGD 2 , 6‐keto‐PGF 1α , 6, 15‐diketo‐PGF 1α or TxB 2 usually had little or no effect 4 PGI 2 antagonized contractions to some excitatory prostanoids, without greatly affecting contractions to acetylcholine 5 For both muscle layers there was a gradient in sensitivity to prostanoids along the gastrointestinal tract. The sensitivities were stomach>distal ileum>sigmoid colon 6 The results are discussed in relation to gastrointestinal physiology and pathophysiology.