EFFECT OF HCL-TREATMENT ON THE CONTRACTILITY OF GUINEA-PIG TRACHEAL SMOOTH MUSCLE

Abstract

It has been known that responsiveness of airway smooth muscle to various contracting substances is enhanced by destruction of epithelium. One of the proposed mechanism is impairment of production of epithelium derived relaxing factor (EpDRF) which is supposed to be produced in epithelial cells. Contraction of guinea-pig airway smooth muscle against acetylcholine (10-4M) was examined before and after the treatment of 1N HCl. One normal HCl (100μl, 300μl or 500μl) was added to 10ml organ bath for 5min in order to cause chemical damage to epithelial cells. No difference was demonstrated in contraction of airway smooth muscle against acetylcholine after the treatment of 100μl 1N HCl. However, contraction was increased from 7.1×10-2g to 8.×10-2g (N=9, p<0.05) after the treatment of 300μl 1N HCl and from 9.2×10-2g to 13.0×10-2g (N=6, p<0.05) after the treatment of 500μl HCl. Dose-response curve against acetylcholine (10-6-10-3M) and histamine (10-7-10-4M) shifted to the left and the maximal contraction increased after the treatment of 300μl 1N HCl. As arachidonic acid metabolite has been reported to be involved in this phenomena, 6keto-PGF1α, a stable metabolite of PGI2 and one of the relaxing prostaglandins, in the organ bath was measured by radioimmunoassay. No significant change in the concentration of 6keto-PGF1α was demonstrated after the treatment of 1N HCl, which indicates that PGI2 is not involved in this phenomenon as EpDRF.