Luke Jeffrey Janssen

Learn More
Excessive airway obstruction is the cause of symptoms and abnormal lung function in asthma. As airway smooth muscle (ASM) is the effecter controlling airway calibre, it is suspected that dysfunction of ASM contributes to the pathophysiology of asthma. However, the precise role of ASM in the series of events leading to asthmatic symptoms is not clear. It is(More)
In general, excitation-contraction coupling in muscle is dependent on membrane depolarization and hyperpolarization to regulate the opening of voltage-dependent Ca(2+) channels and, thereby, influence intracellular Ca(2+) concentration ([Ca(2+)](i)). Thus Ca(2+) channel blockers and K(+) channel openers are important tools in the arsenals against(More)
Asthma is a disease characterised by reversible contraction of airway smooth muscle. Many signalling pathways are now known to underlie that contraction, almost all of which revolve around Ca(2+) handling. Ca(2+) homeostasis in turn is governed by a wide variety of ionic mechanisms, which are still poorly understood. The present review will briefly(More)
1. We investigated the effects of histamine on membrane currents and contractile state of isolated guinea-pig tracheal myocytes using perforated patch and whole-cell recording techniques. The effects of histamine were compared to those of acetylcholine (ACh) and caffeine. 2. During voltage clamp (Vhold = -60 mV), histamine elicited contraction and an inward(More)
Traditionally, the contractile properties of airway smooth muscle have been regarded as its sole contribution to the pathogenesis of asthma. However, our understanding of the role that this structural cell plays in asthma is changing. Airway smooth muscle can undergo hyperplasia and/or hypertrophy leading to structural changes in the airway wall which(More)
Ultimately, asthma is a disease characterized by constriction of airway smooth muscle (ASM). The earliest approach to the treatment of asthma comprised the use of xanthines and anti-cholinergics with the later introduction of anti-histamines and anti-leukotrienes. Agents directed at ion channels on the smooth muscle membrane (Ca2+ channel blockers, K+(More)
1. Membrane currents activated by acetylcholine (ACh) were investigated in isolated canine and guinea-pig tracheal myocytes using the nystatin perforated patch configuration of whole-cell recording. ACh caused depolarization accompanied by a membrane conductance increase. 2. When cells were held under voltage clamp (holding potential, Vh = -60 mV), ACh(More)
We examined the voltage-dependent Ca2+ currents in freshly dissociated smooth muscle cells obtained from canine bronchi (3rd to 5th order). When cells were depolarized from -40 mV, we observed an inward current that 1) exhibited threshold and peak activation at approximately -35 mV and +10 mV, respectively; 2) inactivated slowly with half-inactivation at(More)
Membrane currents and contractions evoked by acetylcholine (ACh) in freshly dissociated canine tracheal myocytes were investigated using the nystatin perforated-patch recording technique. In cells held at -60 mV in the presence of nifedipine, ACh evoked inward current (IACh) and contraction. Caffeine mimicked the effects of ACh. IACh and contractions could(More)
Tetraethylammonium (TEA) 925 mM), 4-aminopyridine (4-AP) (5 mM) and carbachol (3 X 10(-7) M) elicited membrane depolarization (approximately 20 mV) and oscillation (0.5-1.0 Hz; up to 25 mV in amplitude) in canine bronchi (3rd to 5th order). BaCl2 (1 mM) also elicited large depolarizations but not oscillations. The oscillations were antagonized by(More)