Dual Effects of Catecholamines on Pre‐ and Post‐junctional Membranes in the Dog Trachea

Abstract

Effects of noradrenaline or isoprenaline on the membrane and contractile properties of the smooth muscle cell, or on the excitatory neuro‐effector transmission in the dog trachea, in vitro, were observed by use of microelectrodes and double sucrose gap methods. Noradrenaline (<5 × 10−6 m) or isoprenaline (< 5 × 10−7 m) modified neither the membrane potential nor the membrane resistance. Increased concentrations of noradrenaline (> 5 × 10−5 m) depolarized and isoprenaline (> 5 × 10−7 m) hyperpolarized the membrane, and these actions were suppressed by phentolamine and propranolol respectively. Both catecholamines reduced the membrane resistance. Noradrenaline (5 × 10−6 m) or isoprenaline (5 × 10−7 m) reduced the resting tension, raised the mechanical threshold required to produce the contraction and suppressed the amplitude of phasic contractions evoked by electrical depolarization of the membrane. The action potential evoked by an outward current pulse in the presence of tetraethylammonium (TEA) was not affected by 5 × 10−6m isoprenaline, while the mechanical response was markedly suppressed. The excitatory junction potential (e.j.p.) evoked by electrical field stimulation was blocked by atropine. Noradrenaline (5 × 10−7 m) or isoprenaline (5 × 10−8 m) suppressed the amplitude of e.j.p. with no change in the membrane potential or input membrane resistance. Depression in the amplitude of e.j.ps produced by noradrenaline or isoprenaline reduced the amplitude of phasic contractions evoked by e.j.ps. These inhibitory actions of the catecholamines on mechanical responses and on e.j.ps were suppressed by pretreatment with propranolol (4 × 10−6 m). Dog tracheal smooth muscles are innervated by cholinergic excitatory and adrenergic inhibitory systems. Electrical field stimulation produced excitation of both cholinergic and adrenergic nerve fibres, and propranolol (4 × 10−6 m) enhanced the amplitude of e.j.p. generated by excitation of cholinergic nerves when repetitive stimulation (10 stimuli at 20 Hz) was used, but not the amplitude of the e.j.p. evoked by a single stimulus. 5‐Hydroxytryptamine (6 × 10−6 m) produced a tonic contracture of the dog trachea. After pretreatment with atropine (4 × 10−6 m), field stimulation (50 μs in duration and repetitive stimuli at 20 Hz) induced reversal of the contracture induced by 5‐hydroxytryptamine and this was abolished by propranolol (5 × 10−6 m). These results indicate that endogenous or exogenous catecholamines, in relatively low concentrations, predominantly activate β‐adrenoceptors in the pre‐ and post‐junctional membrane in the dog trachea, and induce muscle relaxation.

β‐Adrenoceptor subtypes and the opening of plasmalemmal K+‐channels in bovine trachealis muscle: studies of mechanical activity and ion fluxes

“…That such K+-channel opening is mediated by the activation of P-adrenoceptors is indicated by the ability of propranolol to inhibit the hyperpolarization of airways smooth muscle induced by isoprenaline (Ito & Tajima, 1982;Allen et al, 1985;Honda et al, 1986). However, since propranolol has approximately equal affinity for Pl-and P2-adrenoceptors, this agent does not help in the identification of the P-adrenoceptor subtype responsible for promoting the K+-channel opening.…”

The roles of stored calcium in contractions of cat tracheal smooth muscle produced by electrical stimulation, acetylcholine and high K+

“…In the presence of TEA or procaine, however, depolarizing current-pulses lead to generation of an action potential, as is the case in the dog trachea (Suzuki et al, 1976, Ito & Tajima, 1982. TEA greatly enhances the contractile response, while procaine abolishes the mechanical response.…”

Actions of second messengers synthesized by various spasmogenic agents and their relation to mechanical responses in dog tracheal smooth muscle

“…In the guinea-pig, dog, bovine and rabbit tracheal and bronchial tissues, histamine produces contraction by stimulation of the Hl-receptor, though H2-receptors are also present (Chand & Eyre, 1975;Kirkpatrick, 1975;Kotlikoff et al, 1987). Ito & Tajima (1982) demonstrated that in the dog trachea, isoprenaline produces hyperpolarization of the membrane, reduces the resting tone and relaxes tissues precontracted by ACh. However, in the bovine trachea, isoprenaline stimulates the f2-adrenoceptor and increases Ca influx through activation of the receptoroperated (dihydropyridine-and pertussis toxin-sensitive) Ca channel, whereas isoprenaline reduces Ca influx following pretreatment with carbachol (CCh) (Felbel et al, 1988).…”