Endomorphin-1 and -2 inhibit human vascular sympathetic norepinephrine release: lack of interaction with mu 3 opiate receptor subtype.
OBJECTIVE
To determine if endomorphin-1 (End-1) and -2 (End-2) interact with mu 3 opiate receptor subtype and in this way cause vascular hypotension.


METHODS
Amperometric nitric oxide (NO) determinations associated with opiate binding displacement analysis and preloaded [3H]norepinephrine KCl stimulated release in human vascular tissues from sympathetic nerve fibers in vitro.


RESULTS
The endomorphins did not release NO from human monocytes, granulocytes, saphenous vein, and internal thoracic artery endothelium and did not displace opiate alkaloid binding to mu 3 receptor. However, they did inhibit KCl-stimulated [3H]norpinephrine release from vascular nerves.


CONCLUSIONS
The data strongly suggested that End-1 and -2 caused hypotension by blocking sympathetic vascular sympathetic activity.
Rialas
C M
CM
Multidisciplinary Center for the Study of Aging, State University of New York at Old Westbury 11568-0210, USA.
Fimiani
C
C
Bilfinger
T V
TV
Salzet
M
M
Stefano
G B
GB
D000701:Analgesics, Opioid / Q000494:pharmacology*; D004730:Endothelium, Vascular / Q000378:metabolism; D006801:Humans; D009569:Nitric Oxide / Q000378:metabolism; D009638:Norepinephrine / Q000378:metabolism*; D009842:Oligopeptides / Q000494:pharmacology*; D017450:Receptors, Opioid, mu / Q000819:agonists; D012501:Saphenous Vein / Q000378:metabolism; D013564:Sympathetic Nervous System / Q000378:metabolism; D013895:Thoracic Arteries / Q000378:metabolism
D000701:Analgesics, Opioid; D009842:Oligopeptides; D017450:Receptors, Opioid, mu; C105293:endomorphin 1; D009569:Nitric Oxide; C105294:endomorphin 2; D009638:Norepinephrine