The principle being that it stimulates adenylcyclase
via G proteins, resulting in increased intracellular cyclic AMP which in turn leads to muscle contraction.
The current study confirms previous findings about the role of [beta]-adrenergic receptors in nociception (12, 13), based on decrease of the adenylcyclase
activity (25), reduction of intracellular AMPc and inhibition of voltage sensitive calcium and sodium channels activity (12, 13, 26), which lead to a decrease of neuronal excitability.
Stimulation of these receptors inhibits adenylcyclase via a G protein, thereby reducing intracellular cyclic-adenosinemono-phosphate (c-AMP) concentrations (17).
2]) and thrombin, but in lower concentrations than those required for inhibition of adenylcyclase or stimulation of PLC.
Prostacyclin, released by intact endothelium, inhibits further platelet activation by stimulating adenylcyclase, thereby increasing platelet c-AMP levels.
Even if all the COX-1 is inactivated, platelets will still respond to higher concentrations of other agonists through separate pathways involving adenylcyclase or PLC (Figure 1).
28) Monovalent aurothiolates currently used in medical practice inhibit adenylcyclase
activity in lymphocytes; (29) increase oxygen free radical production in T-cells which results in cellular death following depletion of glutathione; (30) induce the formation of stress proteins in mouse macrophages (31) in response to oxidative stress caused by production of oxygen free radicals; (30) inhibit DNA synthesis in lymphocytes; (32) and suppress immunoglobulin synthesis.