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ANTIDIURETIC HORMONE (ADH) stimulation of urary dramatically creases transepithelial osmotic water permeability (PJ by sertion of unique, highly selective aqueous channels to the apical of granular cells (reviewed Refs. 15, 50). This ADH-elicited crease Pf has been related to the sertion of structures called particle aggregates to the granular cell apical . Before ADH stimulation, the apical Pf is low and particle aggregates are stored dense arrays the limitg s of large cytoplasmic called aggrephores (38). ADH stimulation causes aggrephores to fuse with the granular cell apical and creases Pf. Removal of ADH results a prompt decrease Pf and retrieval of particle aggregates via apical endocytosis (39, 52). previous work, we have used fluorescent and electron-dense markers entrapped with the luma of these retrieved to show that apical endocytosis is responsible for the downregulation of ADHelicited Pf (19, 20). These possessparticle aggregates with their limitg s (6) and, after their recovery from granular cell homogenates, are highly permeable to both water (16) and protons (17), but not other ions. Recently, it has been reported that precubation of (23) and frog (25) urary s with mercurial compounds such as p-chloromercuribenzenesulfonate (pCMBS) hibits ADH-elicited Pf. Likewise, precubation of retrieved apical
AJP - Cell Physiology – The American Physiological Society
Published: Jul 1, 1991
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