The EFFECTS OF Α‐ AND Β‐ADRENOCEPTOR ACTIVATION ON TENSION AND MEMBRANE PROPERTIES OF THE LONGITUDINAL SMOOTH MUSCLE OF THE CHICKEN RECTUM

Abstract

1 Isolated longitudinal muscle strips from the chicken rectum responded to isoprenaline, adrenaline and noradrenaline with a prolonged relaxation. The concentrations required to produce 50% of the maximum relaxation were 1.3 x 10-8 M for isoprenaline, 1.7 x 10-8 M for adrenaline and 10-6 M for noradrenaline. The relaxing potency of isoprenaline is about equal to that of adrenaline, but more than 50 times that of noradrenaline. 2 Propranolol, 3.4 x 10-6 M, blocked the isoprenaline-induced relaxation, and in the presence of this drug the responses to adrenaline and noradrenaline were converted into small, transient relaxations. The residual relaxation was blocked by phentolamine, 2.6 x 10-6 M. 3 These catecholamines suppressed spontaneous spike discharge and produced membrane hyperpolarization. Propranolol, 3.4 x 10-6 M, prevented the inhibitory effects of isoprenaline, and reduced but did not completely abolish those of adrenaline and noradrenaline. 4 Adrenaline and noradrenaline, but not isoprenaline, reduced membrane resistance in some preparations.5 In the rectal muscle of the chicken, the fl-adrenoceptor mediates a prolonged relaxation and the a-adrenoceptor a fast and short-lasting relaxation which is usually obscured by the fl-response and unmasked only after blockade of the P-adrenoceptors. The a-and f-mediated relaxations are each associated with the suppression of spontaneous spike activity.

Nerve pathways involved in adrenergic regulation of electrical and mechanical activities in the chicken rectum

“…The present results show that the transmitter released from the adrenergic nerve terminals produces membrane hyperpolarization which is mediated mainly by P-receptors. Similar effects have been obtained with exogenous adrenaline or noradrenaline in longitudinal muscle strips of the chicken rectum (Komori et al, 1980).…”

“…Similar effects have been obtained with exogenous adrenaline or noradrenaline in longitudinal muscle strips of the chicken rectum (Komori et al, 1980). P-Receptor-mediated membrane hyperpolarization has been shown to be small or absent in intestinal smooth muscles (Bulbring et al, 1980).…”

“…Cessation of spontaneous spike discharges without membrane hyperpolarization can be explained by assuming a pacemaker region for spontaneous spike discharge (Tomita, 1970) in which smooth muscle cells have a high sensitivity to the transmitter associated with a dense distribution of adrenoceptors. If this is the case for these tissues with cable-like properties (Komori et al, 1980), there may occur cells to which spike potentials can be conducted, but membrane hyperpolarization cannot spread.…”

“…has been shown to be small or absent in intestinal smooth muscles (Bulbring et al, 1980). In chicken rectum, P-receptors are of the P2-type (Komori et al, 1980) and it has been demonstrated that preferential release of adrenaline rather than noradrenaline is elicited by stimulation of Remak's nerve trunk (Komori et al, 1979). Thus, this tissue is different from mammalian intestines in which pI-receptors are present (Lands et al, 1967) and noradrenaline functions as the neurotransmitter.…”

Presynaptic, muscarinic inhibition of non‐adrenergic, non‐cholinergic neuromuscular transmission in the chicken rectum

“…This concentration of isoprenaline hyperpolarized the membrane by about 10 mV, but did not alter membrane resistance (Komori et al, 1980a). Fresh drug was frequently added because of its instability in Krebs-Henseleit solution.…”