The effect of some factors on the inhibitory nervous systems of airway smooth muscle

Abstract

To understand better the physiological role of the inhibitory nervous systems (i.e. adrenergic and nonadrenergic) operating in airway smooth muscle, the roles of different physiological conditions were studied using segments of trachea isolated from male guinea pigs (300–400 g BW; Camm-Hartley stain). Laryngeal, cervical and thoracic segments of trachea were used from each animal. Platinum plate electrodes were employed to generate an optimal electrical field stimulation of 40 V, 1.5 msec, 40 PPS of 12 sec duration. Biphasic contractile response was reported as change in the isometric force (g). Adrenergic and nonadrenergic components of airway smooth muscle relaxation were assessed using, D,L-propranolol (1 × 10 −6 M), a dose which did not influence the developed isometric force. We investigated the effect of the following experimental conditions on developed active relaxation: (a) different temperatures (29, 37 and 40°C), (b) pH=7.000, 7.38 and 7.56 (all ±0.05), and (c) moderate hypoxia (PO 2=50±5 Torr). It was found that: (1) No significant differences were detected in the active relaxation in three regions of guinea pig trachea. In guinea pig trechea nonadrenergic inhibition was responsible for approximately 75–80% of total relaxation; (2) A decrease in temperature to 29°C inhibited ( P<0.05) and an increase in temperature to 40°C potentiated ( P<0.01) relaxation in both adrenergic and nonadrenergic components (3) A low pH of 7.10±0.05 inhibited ( P<0.05) and a high pH of 7.56±0.05 potentiated ( P<0.05) relaxation as induced by electrical field stimulation; (4) Acute hypoxia, P O 2 = 50 ± 5 Torr, significantly inhibited ( P < 0.01) active relaxation of tracheal preparations. This inhibition, however, was reversible. These data suggest that in the condition of acidosis and hypoxia, such as is present in patients with chronic obstructive airway disease, the alteration of the inhibitory nervous systems of airway smooth muscle (both adrenergic and nonadrenergic) may contribute to the development of airway obstruction.