HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Iwatsuki, N Articles by Petersen, O H Search for Related Content PubMed PubMed Citation Articles by Iwatsuki, N Articles by Petersen, O H

1. Isolated segments of mouse parotid gland were superfused with a physiological saline solution. Membrane potential and input resistance were measured with intracellular micro-electrodes. Amylase secretion was monitored using an automated fluorometric assay. The parotid gland was stimulated by exposure to isoprenaline (10(-6)M), ACh (10(-6) M), dibutyryl or monobutyryl cyclic AMP (10(-3)M). 2. ACh evoked a sharp decrease in input resistance (from about 3-6 M omega to 1-2 M omega ) accompanied by a modest (two-fold) increase in amylase output. Both effects were fully reversible. 3. Isoprenaline evoked a marked increase in amylase output (five to ten-fold) reaching maximum after 20-30 min of stimulation. Throughout the period of intensive secretion the input resistance remained at the control level. Short pulses of ACh stimulation dramatically reduced input resistance in this period. 4. Dibutyryl cyclic AMP and monobutyryl cyclic AMP caused marked increases in amylase output (five to ten-fold) peaking 40-50 min after start of the continuous stimulation. This increase in amylase secretion was not accompanied by any change in input resistance. Short pulses of ACh stimulation sharply and reversibly reduced input resistance both in control and test periods. 5. It is concluded that the ACh-evoked reduction in input resistance is not a consequence of the secretory event and that secretion does not itself cause a decrease in input resistance.

This article has been cited by other articles:

				D. Heitzmann and R. Warth Physiology and Pathophysiology of Potassium Channels in Gastrointestinal Epithelia Physiol Rev, July 1, 2008; 88(3): 1119 - 1182. [Abstract] [Full Text] [PDF]

				P. Belan, J. Gardner, O. Gerasimenko, J. Gerasimenko, C. L. Mills, O. H. Petersen, and A. V. Tepikin Isoproterenol Evokes Extracellular Ca2+ Spikes Due to Secretory Events in Salivary Gland Cells J. Biol. Chem., April 24, 1998; 273(17): 4106 - 4111. [Abstract] [Full Text] [PDF]

				P. Belan, J. Gardner, O. Gerasimenko, J. Gerasimenko, C. L. Mills, O. H. Petersen, and A. V. Tepikin Isoproterenol Evokes Extracellular Ca2+ Spikes Due to Secretory Events in Salivary Gland Cells J. Biol. Chem., February 13, 1998; 273(7): 4106 - 4111. [Abstract] [Full Text]