{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,28]],"date-time":"2026-03-28T01:54:52Z","timestamp":1774662892668,"version":"3.50.1"},"reference-count":34,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Lung Cellular and Molecular Physiology"],"published-print":{"date-parts":[[1998,3,1]]},"abstract":"<jats:p>The luminal surface of airways is lined by a thin film of airway surface liquid (ASL). Physiological regulation of the depth of ASL has not been reported previously. In this paper, we have used low-temperature scanning electron microscopy of rapidly frozen specimens of bovine tracheal epithelium to demonstrate alterations in the depth of ASL in response to the cholinergic agonist methacholine. We first established that methacholine selectively stimulated airway glands, with maximal secretion at \u223c2 min and a return to baseline within \u223c5 min. A 2-min exposure to methacholine increased the depth of ASL from 23 to 78 \u03bcm. Thereafter, depth decreased linearly with time, reaching 32 \u03bcm at 30 min. The initial increase in depth was blocked by bumetanide, an inhibitor of active chloride secretion, whereas the slow decline back to baseline was inhibited by amiloride, a blocker of active sodium absorption. We conclude that the methacholine-induced changes in ASL depth reflect transient gland secretion followed by liquid absorption across the surface epithelium.<\/jats:p>","DOI":"10.1152\/ajplung.1998.274.3.l388","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T14:03:56Z","timestamp":1514037836000},"page":"L388-L395","source":"Crossref","is-referenced-by-count":18,"title":["Regulation of the depth of surface liquid in bovine trachea"],"prefix":"10.1152","volume":"274","author":[{"given":"D. X.-Y.","family":"Wu","sequence":"first","affiliation":[{"name":"Children\u2019s Hospital Oakland Research Institute, Oakland 94609; Lawrence Berkeley Laboratory, University of California, Berkeley 94720; and Cardiovascular Research Institute, University of California, San Francisco, California 94143"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"C. Y. 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