Endomorphin-1 (Tyr-Pro-Trp-Phe-NH2) and endomorphin-2 (Tyr-Pro-Phe-Phe-NH2) are two endogenous opioid peptides with high affinity and remarkable selectivity for the μ-opioid receptor. The neuroanatomical distribution of endomorphins reflects their potential endogenous role in many major physiological processes, which include perception of pain, responses related to stress, and complex functions such as reward, arousal, and vigilance, as well as autonomic, cognitive, neuroendocrine, and limbic homeostasis. In this review we discuss the biological effects of endomorphin-1 and endomorphin-2 in relation to their distribution in the central and peripheral nervous systems. We describe the relationship between these two μ-opioid receptor-selective peptides and endogenous neurohormones and neurotransmitters. We also evaluate the role of endomorphins from the physiological point of view and report selectively on the most important findings in their pharmacology.

The Endomorphin System and Its Evolving Neurophysiological Role

The airway cholinergic system: physiology and pharmacology.

Functional studies suggest the presence of prejunctional muscarinic autoreceptors on cholinergic nerves in human airways. However, these studies are an indirect method of evaluating changes in neurally evoked acetylcholine (ACh) release. We have investigated the presence of muscarinic autoreceptors in human and guinea pig trachea by comparing the effects of the muscarinic receptor antagonists pirenzepine (M 1 ), methoctramine (M 2 ), 4-DAMP (M 3 ), and rispenzepine (M 1 /M 3 ) on cholinergic neural contractile responses evoked by electrical field stimulation (EFS) and [ 3 H]ACh release. The M 1 , M 1 /M 3 , or M 3 antagonists inhibited the EFS-evoked cholinergic contractile response in a concentration-dependent manner (4-DAMP > rispenzepine > pirenzepine), whereas methoctramine facilitated this response at low concentrations (< 3 μM). In ACh release studies, the M 3 antagonist had no significant effect, whereas pirenzepine, methoctramine, and rispenzepine significantly increased ACh release in guinea pig trachea. In contrast, ACh release was significantly inhibited by the muscarinic agonist oxotremorine M. Methoctramine and the nonselective antagonist ipratropium bromide, but not the M 1 , M 1 /M 3 , or M 3 antagonists, significantly increased ACh release in human trachea. These data suggest the presence of an autoinhibitory receptor on cholinergic nerve terminals in human and guinea pig trachea. In addition, the action of ipratropium bromide at the autoinhibitory receptor may limit its use in the treatment of obstructive airways disease. Patel HJ, Barnes PJ, Takahashi T, Tadjkarimi S, Yacoub MH, Belvisi MG. Evidence for prejunctional muscarinic autoreceptors in human and guinea pig trachea.

Evidence for prejunctional muscarinic autoreceptors in human and guinea pig trachea

From MIF-1 to endomorphin: The Tyr-MIF-1 family of peptides

Inhibitory action of endomorphin-1 on sensory neuropeptide release and neurogenic inflammation in rats and mice.

Modulation of acetylcholine release from parasympathetic nerves innervating guinea-pig and human trachea by endomorphin-1 and -2.

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Modulation of acetylcholine release from parasympathetic nerves innervating guinea-pig and human trachea by endomorphin-1 and -2.