Oscillations in ciliary beat frequency and intracellular calcium concentration in rabbit tracheal epithelial cells induced by ATP.
To investigate how Ca(2+) regulates airway ciliary activity, changes in ciliary beat frequency (CBF) and intracellular calcium concentration ([Ca(2+)](i)) of rabbit tracheal ciliated cells, in response to ATP, were simultaneously quantified with high-speed phase-contrast and fast fluorescence imaging. [ATP]<or= 1 microM induced an increase in [Ca(2+)](i) and CBF that declined to the initial basal levels and was followed by irregular brief increases in [Ca(2+)](i) and CBF. [ATP] > 1 but < 16 microM induced a similar increase in [Ca(2+)](i) and CBF but this was followed by oscillations in CBF and [Ca(2+)](i). The minimum CBF of the oscillations in CBF remained elevated above the basal rate while the minimum concentration of the [Ca(2+)](i) oscillations returned to the basal level. The minimum and maximum CBF of the oscillations in CBF were independent of the [ATP], whereas the frequency of the oscillations in CBF was dependent on the [ATP]. Similar oscillations in CBF and [Ca(2+)](i) were induced by ATP- gamma -S. Although ADP, AMP and adenosine induced a Ca(2+)-independent increase in CBF, neither ATP nor ATP- gamma -S induced an increase in CBF when the Ca(2+) increases were abolished by 20 microM BAPTA AM, a result suggesting that ATP hydrolysis was minimal. [ATP] >or=16 microM induced a sustained elevation in CBF and only a temporary, non-oscillating increase in [Ca(2+)](i). A similar response was induced by thapsigargin (2 microM). Flash photolysis of caged Ca(2+) (NP-EGTA) produced both transient and prolonged increases in [Ca(2+)](i) which were accompanied by transient and sustained increases in CBF, respectively. From these results, we propose that CBF can be increased by a direct Ca(2+) -dependent mechanism that generates the rapid increases in CBF associated with the oscillations or by an indirect Ca(2+)-dependent mechanism that is responsible for the sustained minimum increase in CBF.
Zhang
Luo
L
Department of Physiology, University of Massachusetts Medical School, Worcester, MA 01655, USA.
Sanderson
Michael J
MJ
D000255:Adenosine Triphosphate / Q000031:analogs & derivatives* / Q000494:pharmacology*; D000818:Animals; D002021:Buffers; D002118:Calcium / Q000378:metabolism*; D002478:Cells, Cultured; D002614:Chelating Agents / Q000494:pharmacology; D002923:Cilia / Q000187:drug effects / Q000502:physiology*; D004533:Egtazic Acid / Q000031:analogs & derivatives* / Q000494:pharmacology; D006868:Hydrolysis; D007425:Intracellular Membranes / Q000187:drug effects / Q000378:metabolism*; D009991:Oscillometry; D009994:Osmolar Concentration; D011817:Rabbits; D020545:Respiratory Mucosa / Q000166:cytology / Q000378:metabolism*; D013997:Time Factors; D014132:Trachea / Q000166:cytology / Q000378:metabolism*
D002021:Buffers; D002614:Chelating Agents; C070379:1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester; C022571:adenosine 5'-O-(3-thiotriphosphate); D004533:Egtazic Acid; D000255:Adenosine Triphosphate; C025603:1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid; D002118:Calcium