Abstract

Carotid artery and aorta homogenates synthesized epinephrine (E) from norepinephrine (NE) in the presence of S-adenosylmethionine. Aorta synthesized epinine by the N-methylation of dopamine (DA) about 3 times as well as it synthesized E from NE. In contrast, adrenal homogenates which contain phenylethanolamine N-methyltransf erase (PNMT) methylated DA only 1% as well as NE. The PNMT inhibitor SKF 29661 h a d no significant effect on methylation of NE by aorta but inhibited adrenal PNMT b y 88%.

N-Methylating activity in arterial homogenates was increased by dexamethasone and following catecholamine depletion by 6-hydoxydopamine (6-OHDA) and reserpine.

Nine days after adrenal demedullation blood E levels collected at decapitation were less t h a n 7% of levels found in sham operated controls but artery homogenate E was unchanged. Demedullated rats given 6-OHDA followed by reserpine for 4 days also had unchanged arterial E levels despite arterial NE levels that were less t h a n 15% of controls.

We conclude that arteries synthesize E in vitro and appear to synthesize E in vivo using an extraneuronal 2V-methyltransferase. This enzyme differs from adrenal PNMT in substrate and inhibitor specificity and its activity is enhanced by catecholamine depletion and by glucocorticoid treatment. Am J Hypertens 1991:4:45–50

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