Opioid Receptor Modulation of Neural Transmission in the Rabbit Coeliac Ganglion and Ganglionic Opioid Receptor Activation by Bunitrolol

Abstract

1. We examined the preganglionic splanchnic nerve activity and postganglionic renal nerve activity before and after a local injection of naloxone (20 &kg) into the coeliac ganglion of anaesthetized rabbits. This was done during graded hypertension, induced by the administration of phenylephrine (0.5-10 kg/kg, i.v.) and with selective intraganglionic injection of methionine-enkephalin (ME) and bunitrolol, which is a beta-blocker.2. During hypertension both pre-and postganglionic discharge decreased, but only postganglionic discharge was inhibited by naloxone treatment into the ganglion.3. Local injection of ME (0.1-10 pg/kg) into the coeliac ganglion decreased postganglionic activity by 9.0 f 1 .O to 4 I .2 ? 4.7% from control, and this decrease was inhibited by naloxone. Administration of bunitrolol( 1-300 @kg) decreased postganglionic discharge by 3 . 9 t 1.4 to 39.7 +2.4% of the control and this decrease was also inhibited by naloxone.5. These results suggest that opioid receptors in the coeliac ganglion play an inhibitory role in neural ganglionic transmission and that this inhibitory action reduces postganglionic sympathetic discharge.

Chronic μ-Opioid Receptor Stimulation in Humans Decreases Muscle Sympathetic Nerve Activity

“…43 Furthermore, celiac ganglionic neural discharge and superior cervical ganglionic acetylcholine release are decreased by local administration of the opioid receptor ligand methionine-enkephalin, indicating inhibition of sympathetic ganglionic transmission to multiple organ systems. 44,45 The mechanism for increased epinephrine plasma concentration during chronic opioid administration in our patients remains unclear. Possibly, adrenal epinephrine release is less sensitive to the inhibitory effects of chronic opioid agonist administration or, in contrast to the decrease in MSA, shows a compensatory increase.…”

The Influence of Captopril and Naloxone on the Valsalva Manoeuvre and Systolic Time Intervals in Healthy Volunteers

“…A11 levels were not measured and its effect in our study remains speculative. Although A11 possibly has a direct inotropic effect on the heart (Koch-Weser 1965;Freer et al 1976), and enkephalin supposedly inhibits sympathetic discharge (Araujo & Collier 1978;Horiuchi et al 1989), we could not demonstrate a reduction in cardiac inotropism with captopril using Q S L No effect of A11 on venous capacitance (Flapan et al 1992;Motwani & Struthers 1992) was evident from the preload-sensitive STI, PEP index and PEP/LVET (Buch et al 1980).…”

“…Enkephalin has been demonstrated to act as a transmitter substance (Del Fiacco et al 1985;Jarvi et al 1988) which presynaptically inhibits the release of acetylcholine in the sympathetic ganglia (Araujo & Collier 1987) and therefore reduces sympathetic stimulation (Konishi et al 1981;Horiuchi et al 1989). Methionine-enkephalin induced inhibition of post ganglionic discharge in the rabbit (Horiuchi et al 1989) and in the isolated superior cervical ganglion of the cat (Araujo & Collier 1987) was reversed by naloxone thus implying the presence of preceptors. ACE inhibition has been shown to inhibit the degradation of enkephalin by inhibiting the 'enkephalinase' enzyme (Marcello et al 1986;Altstein et al 1987;Lantz et al J. I?…”