Effects of relaxants on electrical and mechanical activities in the guinea‐pig tracheal muscle

Abstract

1 In isolated tracheal musces of the guinea-pig, effects of several relaxants were studied by simultaneously recording the membrane potential and mechanical response. 2 Intracellular recordings showed regular slow waves in most preparations. There was a close correlation between membrane potential and slow wave amplitude. The linear regression line of the slow wave amplitude (Y mV) on the membrane potential (X mV) could be expressed by Y = -0.35X -5.9. The mean values of resting potential and slow wave amplitude were -50.6 ± 0.6 m.V a-nd 11.9 ± 0.5 mV, respectively. 3 Relaxant drugs used (isoprenaline, terbutaline, adrenaline, noradrenaline, theophylline, forskolin and dibutyryl cyclic AMP) all produced hyperpolarization of the membrane and abolished the slow wave. The degree of relaxation was closely related to these electrical responses, although the recovery of electrical responses was faster than the mechanical response. 4 It was concluded that the relaxation caused by the agents, which are known to increase the intracellular cyclic AMP level, was accompanied by a clear hyperpolarization and suppression of slow waves.

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.…”

Effects of Excess K+ on Carbachol-induced Contractions in the Guinea-Pig Tracheal Muscle.

“…This potentiation could be explained by a decrease in driving force for Ca2+ influx or if the receptor-mediated pathway was inhibited by membrane depolarization, or if the receptor-mediated pathway had become more susceptible to the dihydropyridines when the channels has been described previously (Nelson et al, 1989), but it seems unlikely that such an effect would contribute to our observations. The membrane potential of bronchial smooth muscle is about -50mV in control solutions (Ahmed et al, 1985;Honda et al, 1986), and of those which make dihydropyridines inactive.…”

Comparative effects of BRL 38227, nitrendipine and isoprenaline on carbachol‐ and histamine‐stimulated phosphoinositide metabolism in airway smooth muscle

“…It has been known for sometime that 13-adrenoceptor agonists also cause hyperpolarization of tracheal smooth muscle (Allen et al,, 1985;Honda et al, 1986) through a covalent modification of the Ca2+-dependent K+-channel by adenosine 3':5'-cyclic monophosphate (cyclic-AMP)-dependent protein kinase (Kume et al, 1989). In common with the observed effects of K+-channel openers, the Padrenoceptor agonist-induced hyperpolarization approaches the K+ equilibrium potential (Allen et al, 1985;Honda et al, 1986). However, the P-adrenoceptor effect on transmembrane potential is not required for the relaxant response (Allen et al, 1985) and the failure of elevated [K+] (Coburn & Baron, 1989;Worley & Kotlikoff, 1990), the importance of such channels as mediators of the maintained Ca2'-influx response to spasmogens is still uncertain (Murray & Kotlikoff, 1991).…”