Presynaptic opioid delta‐receptors in the rabbit mesenteric artery.

Abstract

Excitatory junction potentials (e.j.p.s) evoked by nerve stimulation were recorded from muscle cells of the rabbit isolated mesenteric artery. At 0.03 Hz the e.j.p. amplitudes were stable. When a train of fifteen pulses was applied at 0.25 Hz or at higher frequencies (0.5, 1 and 2 Hz), e.j.p.s showed an initial facilitation followed by depression. [Met5]enkephalin 0.1 and 1 mumol/l, [D‐Ala2,D‐Leu5]enkephalin 0.1 and 1, but not 0.01 mumol/l, and [D‐Pen2, L‐Pen5]enkephalin 3 mumol/l all depressed the e.j.p.s evoked by trains of fifteen pulses at 1 Hz. When more than one concentration was used ([Met5]enkephalin, [D‐Ala2,D‐Leu5]enkephalin), the inhibition was concentration dependent. It was always greater for the first few e.j.p.s than for the later ones in a train. [Met5]enkephalin 1 mumol/l reduced the first e.j.p. at 1 Hz and the e.j.p.s evoked by 0.03 Hz to a similar extent. The inhibitory effect of [Met5]enkephalin 1 mumol/l on e.j.p.s persisted in the presence of yohimbine 0.3 mumol/l. Naloxone 1 mumol/l did not interfere with the effect of [Met5]enkephalin 1 mumol/l. Naloxone 10 mumol/l depressed some e.j.p.s and prevented the inhibition by [Met5]enkephalin 1 mumol/l. Neither ICI 154129 10 mumol/l nor ICI 174864 0.3 mumol/l had any effect of their own and both compounds antagonized the action of [Met5]enkephalin 1 mumol/l. Normorphine 10 mumol/l, fentanyl 1 mumol/l, ethylketocyclazocine 0.1 mumol/l, and dynorphin A(1‐13) 1 mumol/l were all ineffective. Ethylketocyclazocine 1 mumol/l did not change the e.j.p.s either, but antagonized [Met5]enkephalin 1 mumol/l. [Met5]enkephalin 1 mumol/l failed to influence both the resting membrane potential of the muscle cells and the depolarizing effect of noradrenaline 3 and 30 mumol/l. We suggest that the axon terminals of post‐ganglionic sympathetic neurones in the rabbit mesenteric artery possess opioid delta‐, but not mu‐ or kappa‐receptors. The activation of presynaptic delta‐receptors inhibits the release of the neuroeffector transmitter. There is no evidence for any effect of co‐released endogenous opioid peptides under our experimental conditions.

Opioid Receptor Blockade Improves Mesenteric Responsiveness in Biliary Cirrhosis

“…(* P \ 0.05 cirrhotic/saline group in comparison with Sham/saline group) cardiovascular system. However, arterial nerves of mesenteric vascular bed are also known to express d-opioid receptors [13], activation of which can result in a decrease neuroeffector release and consequent neurogenic hyporesponsiveness. Opioid induced increase in NO production has been well characterized previously.…”

Change in Opioid Peptide Level in the Heart and Blood Plasma During Acute Myocardial Ischaemia Complicated by Ventricular Fibrillation

“…Such effect of D-AlaZ,LeuS,Ar@-enkephalin may be based on enkephalins ability to inhibit catecholamines release from sympathetic terminals (Caffrey 1984;Caffrey et al 1985;Illes et al 1986), for there is evidence testifying to the key role of catecholamines in heart rhythm disturbances in AM1 (Lubbe et al 1976;Botting et al 1983;Lombarde et al 1983;Lubbe et al 1987). We have previously shown (Alekminskaya et al 1986) that dalargin pretreatment before AM1 prevents an increase of activity of the sympathetic nervous system.…”

“…Some reports, however, concentrate on the ability of enkephalins to restrict norepinephrine release from sympathetic nerve endings by their influence on presynaptic opiate receptors on sympathetic terminals (Caffrey 1984;Caffrey er al. 1985;Illes et al 1986). This testifies to the ability of opioid peptides to decrease the possibility of arrhythmia in coronary artery occlusion by de-creasing the adrenergic effect on myocardium.…”

Influence of Opioids in Hypothalamic Nuclei on Cold Thermogenesis of Lean and Obese LA/N‐cp Rats

“…As an example, circulating catecholanines (12) and muscle sympathetic nerve activity (11) are higher during exercise when opioid receptors are antagonized. Other lines of evidence support <an inhibitory role for opioids on the SNS (22); however, Van Loons' group has demonstrated a stirnulatory effect on circulating catecholamines when beta endorphin is infused into the hypothalamus of normal weight rats (2,s 1).…”