Abstract
Arachidonic acid, which is esterified mainly at the Sn-2 position of phospholipids, is deacylated in response to a wide variety of neurohormonal stimuli, including sympathetic nerve stimulation and catecholamines. In most cardiovascular tissues, arachidonic acid is metabolized via the cyclooxygenase pathway into prostaglandins. The kind and quantity of prostaglandins formed in response to adrenergic stimuli vary in different tissues. For example, PGE2 is the major product of arachidonic acid formed in the spleen and kidney and PGI2 in the heart in response to sympathetic nerve stimulation and norepinephrine. The sequence of events, including the type of adrenergic receptor involved in the action of catecholamines on PG synthesis, varies from tissue to tissue. For example, PG synthesis elicited by adrenergic stimulation in the heart is mediated via activation of beta-1 adrenergic receptors, whereas in the kidney it is linked to stimulation of alpha-1 adrenergic receptors. Moreover, prostaglandin synthesis elicited by alpha-1 adrenergic receptor activation in the kidney requires only partially extra- but mainly intracellular Ca++ and calmodulin. However, beta-1 adrenergic receptor stimulated PG synthesis in the heart is absolutely dependent upon extracellular Ca++ but not on calmodulin. Furthermore, alpha-1 but not beta-1 adrenergic receptor stimulated PG synthesis is inhibited by mepacrine, a phospholipase A2 and C inhibitor.(ABSTRACT TRUNCATED AT 250 WORDS)
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