Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We present a case of cutaneous vasculitis apparently due to an adverse reaction to atenolol. The causal relationship between the drug and the eruption was based mainly on circumstantial evidence. It has been further strengthened by positive results of the indirect rat mast cell degranulation test. The number of published cases of reaction to atenolol is limited. Cutaneous vasculitis has, to the best of our knowledge, never been reported as an adverse reaction to atenolol, although it is not a rare side effect of other beta blocker drugs including propranolol and practolol. Atenolol should be added to the list of beta blocker medications that may produce cutaneous vasculitis.
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PMID:Atenolol-induced cutaneous vasculitis. 252 89

The lipophilic beta-adrenoceptor blocking (BAB) drugs metipranolol, propranolol and exaprolol significantly decreased 48/80- and A23187-induced 32P incorporation into rat mast cell phospholipids. Exaprolol was the most active, followed by propranolol and metipranolol. Atenolol and metipranolol significantly decreased the 48/80-stimulated, and metipranolol and exaprolol the A23187-stimulated 3H-arachidonic acid liberation from isolated mast cells.
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PMID:Effect of beta-adrenoceptor blocking drugs on 32P incorporation into and arachidonic acid liberation from phospholipids in stimulated rat mast cells. 256 43

The effect of betaadrenoceptor blocking drugs atenolol and propranolol was studied in both nonstimulated and stimulated isolated rat mast cells. Atenolol did not liberate histamine from non-stimulated mast cells, decreased spontaneous secretion, inhibited 48/80 stimulated histamine release, increased 32P incorporation into membrane phospholipids, decreased membrane fluidisation and decreased arachidonic acid liberation from membrane phospholipids of stimulated mast cells. Propranolol dose-dependently liberated histamine from nonstimulated mast cells and inhibited histamine liberation, it nonsignificantly increased membrane phospholipid turnover but significantly increased membrane fluidisation and inhibited stimulated arachidonic acid liberation in stimulated mast cells. The results indicated the interaction of atenolol and propranolol with mast cell membranes, particularly with the phospholipid bilayer, resulting in a possible inhibition of phospholipase A2 activation. Histamine liberation suggested its displacement from granule binding sites after intracellular propranolol accumulation in mast cells.
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PMID:Pharmacology of histamine liberation. Cationic amphiphilic drugs and mast cells. 753 Oct 10