[Influence of stimulation and inhibition of adrenergic receptors on ion transport in isolated rabbit trachea in electrophysiologic investigations].
Components of neural system in airways interact, and activation of one neural path can influence the releasing of mediators in other neural path. Electrophysiological investigations of mediators-influenced ion transport are one of many possibilities to study interactions between neural system in airway and airway's epithelium. Electrical transepithelial potential difference (PD) and transepithelial resistance (R) of isolated rabbit's tracheal wall were measured by using classical Ussing's method. Two types of stimulations applied on the tracheal mucosa were estimated; namely, the stimulation of adrenergic receptors by epinephrine (AD) and the mechanical stimulation (MS) by stream of fluid. The tissue reacted to both types of stimulations or was unresponsive in relation to both stimulations (Tab. 1). Changes of PD were reactions to AD or MS, whereas R remained without changes (Tab. 1 and 4). Ionic composition of the medium mimicked the composition of extracellular organism fluid. In such medium AD caused persistent depolarization of PD, whereas MS caused transient hyperpolarization of PD (Fig. 1). Regitin (RG) blocker of alpha-adrenergic receptors, beta-blocker propranolol (PR), and inhibition of prostaglandins synthesis by indomethacin diminished reaction of tracheal wall to AD (Tab. 2 and 3). Inhibition of chloride ions secretion by bumetanide diminished the reaction to AD, and lowered reaction to MS (Tab. 2). Inhibition of sodium ions absorption by amiloride had no influence on reaction after AD or after MS (Tab. 2). Indomethacin diminished reaction of the tissue to AD, while the reaction to MS remained without changes (Tab. 2). During the action of AD, RG, or PR reaction of tracheal wall to MS was upheld (Fig. 2, Tab. 4). Maintenance of reaction to MS despite previous influence on adrenergic receptors suggests that the epithelial cells, on the one hand, can be under adrenergic control and react in a manner being dependent on adrenergic system, and on the other hand they can independently respond to exogenous stimuli.
Wojciechowska
I
I
Zakładu Patofizjologii, Pomorskiej Akademii Medycznej w Szczecinie.
D000322:Adrenergic Agonists / Q000494:pharmacology; D018674:Adrenergic Antagonists / Q000494:pharmacology; D000818:Animals; D002034:Bumetanide / Q000494:pharmacology; D004594:Electrophysiology; D004837:Epinephrine / Q000378:metabolism / Q000494:pharmacology; D005260:Female; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D017136:Ion Transport / Q000187:drug effects / Q000502:physiology*; D008297:Male; D010646:Phentolamine / Q000494:pharmacology; D010812:Physical Stimulation; D011433:Propranolol / Q000494:pharmacology; D011817:Rabbits; D011941:Receptors, Adrenergic / Q000187:drug effects / Q000378:metabolism*; D013268:Stimulation, Chemical; D014132:Trachea / Q000378:metabolism*
D000322:Adrenergic Agonists; D018674:Adrenergic Antagonists; D011941:Receptors, Adrenergic; D002034:Bumetanide; D011433:Propranolol; D007213:Indomethacin; D004837:Epinephrine; D010646:Phentolamine