Possible Interaction: Arachidonic Acid and Propranolol

“Treatment of hypertensive patients with dl-propranolol (640 mg/day) significantly inhibited thromboxane synthesis by their platelets and platelet aggregation induced by thrombin or arachidonic acid.”

“Beta blockers may have this effect through phospholipase A2 because the conversion of exogenous arachidonic acid to TxB2 was not affected except in the case of propranolol , which inhibited slightly TxB2 formation from exogenous arachidonic acid.”

“Pretreatment of cells with the phosphatidate phosphohydrolase blocker, propranolol , significantly enhanced the carbachol-induced elevation of phosphatidic acid, but decreased agonist-stimulated production of diacylglycerol and arachidonic acid , indicating that phosphatidlycholine was the likely source of arachidonic acid.”

“Inhibitors of PLD (C2 ceramide), phosphatidate phosphohydrolase propranolol ), and diacylglycerol lipase (RHC 80267) attenuated Ang II–induced arachidonic acid release.”

“ Propranolol also increased the production of PA in the presence of Ang II by 320% and reduced DAG and arachidonic acid (AA) accumulation.”

“ATP significantly stimulated arachidonic acid release in a dose-dependent manner in the range between 0.01 and 0.5 mmol/L. DL-Propranolol hydrochloride (propranolol), an inhibitor of phosphatidic acid phosphohydrolase, significantly inhibited the ATP-induced release of arachidonic acid.”

“ET‐1 stimulated arachidonic acid release dose‐dependently in the range between 0.1 nM and 0.1 μM. Propranolol , an inhibitor of phosphatidic acid phosphohydrolase, significantly inhibited the ET‐1‐induced arachidonic acid release in a dose‐dependent manner as well as the ET‐1‐induced diacylglycerol formation.”

“Ang II significantly stimulated AA metabolite release in a concentration-dependent manner in the range between 1 nmol/I and 0.1 mumol/I. D.L.-Propranolol hydrochloride (propranolol), an inhibitor of phosphatidic acid phosphohydrolase, significantly inhibited the Ang II-induced release of AA metabolites.”

“The phosphatidic acid phosphatase (PAPase) inhibitor propranolol , inhibiting the generation of diacylglycerol (DAG) and further AA from phosphatidic acid (PA), could totally down‐regulate the IFN‐γ‐induced release of AA.”

“ Propranolol (PRO), alprenolol (ALP), metipranolol (MET) and oxprenolol (OXP) inhibited arachidonic acid (AA) liberation from membrane phospholipids, malondialdehyde (MDA) formation and thromboxane B2 (TXB2) production in stimulated platelets.”