Electromechanical coupling in canine trachealis muscle: acetylcholine contractions

Abstract

Organ bath and double sucrose gap experiments were performed on strips of canine trachealis muscle. With a slow increase in acetylcholine (ACh) concentration to 2 .times. 10-5 M, onset of membrane depolarization coincided with onset of development of tension, and tension changes roughly paralleled membrane potential changes. Quasi-steady-state membrane depolarization-tension plots showed shifts in ACh data compared to elevated K+ data, so that ACh membrane depolarization for a given tension was smaller than seen during elevated K+ contractions, Verapamil, D-600 [.alpha.-isopropyl-.alpha.-[(N-methyl-N-homoveratryl)-.alpha.-aminopropyl]-3,4,5-trimethoxyphenylacetonitrile] and La3+ completely inhibited K+ contractions, but ACh contractions were resistant to these agents. During ACh contractions, plasma membrane hyperpolarization evoked with anodal current pulses resulted in contractions, and evoked depolarization usually resulted in relaxation. These anomalous tension responses to current injection were unchanged by verapamil, D-600 or La3+ (at concentrations that completely inhibited K+ contractions), or by tetrodotoxin or propranolol. During K+ or 5-hydroxytryptamine (5-HT) contractions, current injection gave tension responses that suggested electromechanical coupling mechanisms were operative. Membrane potential-dependent increases in plasma membrane Ca2+ transport that occur during K+ contractions are inactivated or not activated during ACh contractions. ACh contractions appear to be largely independent of ACh membrane depolarization in contrast to K+ and 5-HT contractions in which electromechanical coupling is evident and membrane potential-dependent Ca2+ transport operative.