The OCCURRENCE OF POSTSYNAPTIC Α‐ AND Β‐ADRENOCEPTORS IN THE GUINEA‐PIG GALL BLADDER

Abstract

I Guinea-pig gall bladder strips were contracted by (--noradrenaline, 10-5 M, and by field stimulation at 5 Hz (in the absence or presence of 10-6 M atropine) and relaxed to 10-s M (--isoprenaline. (-)-Adrenaline, 10-5 M, predominantly contracted, but sometimes relaxed, this preparation. 2 In the presence of 10-6 M phentolamine, contractions to (--noradrenaline and to (-)-adrenaline were reversed to relaxations. The relaxations produced by (-)-isoprenaline were unaltered. In the presence of 10'6 M propranolol, contractions to (-)-noradrenaline increased in magnitude, relaxations to (-)-adrenaline were reversed to contractions, and relaxations to (-)-isoprenaline were abolished. These results demonstrate the presence of postsynaptic ax-adrenoceptors which mediate contractions, and postsynaptic ,B-adrenoceptors which initiate relaxations, in the guinea-pig gall bladder. 3 The contractile responses to continuous field stimulation for 5 min at 5 Hz in Krebs solution alone were reduced in magnitude by propranolol, 10-6 M. In the presence of 10-6 M atropine (added to eliminate the cholinergic component of the response), propranolol, 1lo' M, had no effect on responses to stimulation at 5 Hz. Thus propranolol reduced the response to cholinergic stimulation in this tissue; the basis of this effect is unclear. In the absence or presence or atropine (10-6 M), the responses to 5 Hz were smaller in magnitude in the presence than absence of phentolamine, 10-6 M. This suggests that the responses to field stimulation of the guinea-pig gall bladder may, in part, be due to the release of endogenous noradrenaline which acts at postsynaptic a-adrenoceptors.

Relaxation of canine gallbladder to nerve stimulation involves adrenergic and non‐adrenergic non‐cholinergic mechanisms

“…5Hz) did not activate adrenergic nerves, because the relaxations remained the same in presence of guanethidine. Both inhibitory (β) and excitatory (α1) adrenergic receptors have been described in gallbladder smooth muscle 24 . As expected, blocking of β‐receptors by propranolol reduced adrenergic‐sensitive relaxations during EFS but, in agreement with the results obtained in the presence of guanethidine, propranolol failed to reduce the relaxing response to 5 Hz EFS.…”

“…Both inhibitory (b) and excitatory (a1) adrenergic receptors have been described in gallbladder smooth muscle. 24 As expected, blocking of b-receptors by propranolol reduced adrenergic-sensitive relaxations during EFS but, in agreement with the results obtained in the presence of guanethidine, propranolol failed to reduce the relaxing response to 5 Hz EFS. In the cat gallbladder, Chen et al 19 reported that adrenergic ®bres, releasing norepinephrine and acting on b-adrenergic receptors on the gallbladder muscle, were the only mediators of postganglionic intramural neurone stimulation by EFS.…”

Noradrenaline as a presynaptic inhibitory neurotransmitter in ganglia of the guinea‐pig gall‐bladder.

“…Electrical stimulation of the splanchnic or coeliac nerves results in a decrease in the tone of the gall-bladder that is sometimes preceded by a brief contraction (Pallin & Skoglund, 1964;Persson, 1972Persson, , 1973Yamasato & Nakayama, 1990). Application of noradrenaline can also result in relaxations and/or contractions, depending on the experimental conditions (Persson, 1972(Persson, , 1973Doggrell & Scott, 1980;Dahlstrand et al 1989).…”

Prokinetic effect of indoramin, an α‐adrenergic antagonist, on human gall‐bladder

“…Studies in vitro in non‐human species indicate that gall‐bladders express post‐synaptic α‐, β 1 ‐ and β 3 ‐receptors, 6 , 7 and that, in general, β 1 ‐ and β 3 ‐stimulation produces relaxation of the gall‐bladder smooth muscle, whereas post‐synaptic α‐stimulation mediates contraction 8 . However, there have been no previous studies performed demonstrating the effects of adrenergic control on human gall‐bladder motility in vivo .…”