Endomorphin-1 and -2 inhibit human vascular sympathetic norepinephrine release: lack of interaction with mu 3 opiate receptor subtype.

Aim: 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.

Conclusion: The data strongly suggested that End-1 and -2 caused hypotension by blocking sympathetic vascular sympathetic activity.