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.