Doctoral Dissertations

Date of Award

6-1983

Degree Type

Dissertation

Degree Name

Doctor of Philosophy

Major

Zoology

Major Professor

John R. Kennedy

Committee Members

Jeff McCabe, Gerald Vaughan, John Abel, Kermit Duckett

Abstract

Both calcium and cyclic adenosine 3',5'-monophosphate appear to play a role in the reflation of ciliary activity in rabbit tracheal epithelium. Elevation of cellular calcium levels using calcium ionophore A23I87 stimulates ciliary motility in both explant and outgrowth cells. Prolonged exposure of the cells to A23I87 leads to a reduction in ciliary frequency and ultimately to cessation. Reactivation studies utilizing demembranated ciliated cortices suggest that high levels of Ca2+ may act directly on the axoneme to exert an inhibitory effect on motility.

Depletion of cellular calcium by exposure to A23I87 plus EGTA caused an immediate reduction in ciliary activity in explant and outgrowth cells. This may be due to a detrimental effect on mitochondria since the studies using demembranated models suggest that calcium is not necessary for reactivation of cilia.

Exposure of intact ciliated cells to theophylline and cholera toxin, agents which have been reported to elevate cellular cAMP levels, and to 8-Br cAMP, a cAMP analog, results in an increase in ciliary frequency. Direct exposure of the ciliary axoneme to cAMP using demembranated ciliary preparations causes enhanced ciliary amplitude and increased duration of reactivation.

Neither calcium nor cAMP are necessary for initiation or maintenance of ciliary motility but probably act to modulate ciliary activity. The interaction between calcium and cAMP in the control of ciliary motility is unknown but the present investigation suggests that increased intracellular calcium may stimulate cellular cAMP production and in turn increase ciliary frequency.

Tracheal epithelium is a sodium-transporting tissue and the movements of sodium and calcium in this tissue appear to be interrelated. In the presence of veratridine, an alkaloid which has been shown to elevate sodium levels in some cells, 45Ca uptake is increased and coincides with a stimulation of ciliary frequency. Ouabain, which causes an increase in cellular sodium levels through an inhibition of Na+K+ATPase, reduces ciliary activity but calcium fluxes are unchanged. Unlike ouabain, veratridine causes increased intracellular sodium levels in the presence of functioning Na+K+ATPase. Therefore cellular K+ levels should be unaltered by veratridine and the difference between the effects of these two drugs on ciliary motility and cellular calcium levels may be related to intracellular K+ levels. The stimulation of ciliary frequency by veratridine may be the result of increased intracellular calcium as for cilia exposed to A23I87. Exposure of the ciliated epithelium to depolarizing concentrations of extracellular K+ or to Na+-free medium, does not affect ciliary frequency.

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