AJP - Regulatory, Integrative and Comparative Physiology, Vol 264, Issue 1 162-R168, Copyright © 1993 by American Physiological Society
Secretagogue-induced 86Rb+ efflux from bovine parotid is HCO3- dependent
S. I. Lee and R. J. Turner
Clinical Investigations and Patient Care Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892.
Muscarinic agonist (carbachol)-induced K+ loss from a bovine parotid mince
was studied using 86Rb+ as a K+ marker. In contrast to our previous studies
with the rat parotid [Am. J. Physiol. 261 (Gastrointest. Liver Physiol.
24): G111-G118, 1991] in which both Cl(-)-dependent and HCO3(-)-dependent
components of carbachol-induced 86Rb+ efflux were observed, no significant
evidence for Cl(-)-dependent 86Rb+ loss was detected in the bovine parotid.
HCO3(-)-dependent agonist-induced 86Rb+ loss was blunted by K+ and Cl-
channel blockers and by removal of extracellular Ca2+, consistent with the
hypothesis that this 86Rb+ loss occurs via a Ca(2+)-activated K+ channel
and that this cation loss serves to electrically balance the concomitant
loss of HCO3- via an electrically conductive pathway, presumably an apical
anion channel. Acetate, formate, and propionate could substitute for HCO3-.
Interpreted in terms of current models of salivary fluid secretion, which
hypothesize that the production of fluid is secondary to anion secretion
accompanied by an electrically coupled K+ loss, these results indicate that
salivary production in the bovine parotid is driven almost exclusively by
acinar HCO3- secretion.
