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KMID : 0370819920070010001
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Yonsei Journal Dental Science
1992 Volume.7 No. 1 p.1 ~ p.18
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EFFECTS OF CAFFEINE ON THE CARBACHOL-INDUCED K+ RELEASE IN RAT PAROTID ACINI
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신동민
김석현/배지명/이은하/김순이/이승일
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Abstract
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The stimulation of the muscarinic receptor in salivary gland causes the increase in the intracellular calcium (Ca2+) level via inositol trisphosphate (IP3). In regards of Ca2+ mobilization, the existence of IP3-insensitive Ca2+ pool (IICP) has
been
reported. In addition, close intercommunication between caffeine (CAF)-sensitive Ca2+ pool (CSCP) and IP3-sensitive Ca2+ pool (ISCP) has been proposed to account for the mechanism of intracellular Ca2+ mobilization. In this study, the effect of
caffeine
on the Ca2+ mobilization was examined in rat parotid gland.
The parotid minced tissue was placed in the perifusion chamber with the K+-sensitive electrode. To stimulate the parotid acini, carbachol was perifused with Krebs Ringer bicarbonate (KRB) solution. As a result, in parotid acini,
tetraethylammonium
(TEA
; 5 mM), the blocker of Ca2+-activated K+ channel, inhibited CCh (10-5 M)-induced K+ release by 52.35±3.61%. Under the condition of prior exposure to CAF (10 mM), CCh-induced K+ release was reduced by 68.95±3.61% of the effect caused by CCh
alone.
Furthermore, the removal of CAF after exposure to CCh and CAF caused another increase in CCh-induced K+ release, which corresponded to 44.30±7.19% of initial condition (CCh plus CAF).
Such an increase in CCh-induced K+ release by removal of CAF from the solution with CCh and CAF, was not only related to external Ca2+, but also not affected by the exposure to Ni2+ and Mn2+ which are Ca2+ channel blockers. Nevertheless, ouabain
(1
mM),
blocked CCh-induced K+ releases caused by the omission of CAF by the 90.80±1.69%. In contrast, CCh-induced K+ efflux (initial rate of K+ release) was remarkbly blunted by the removal of CAF, compared with that in the presence of the CCh and CAF,
which
was indenpedent of the Ca2+ in the external medium. Taken all together, these results suggest that 10 mM caffeine is able not only to release Ca2+ from the intracellular pool, but also to block somewhere the process of Ca2+ release when cells are
stimulated withcaffeine. Furthermore, Ca2+-activated CCh-induced K+ release might be closely associated with the intracellular Na+ concentration.
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KEYWORD
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