A Ca2+-sensing receptor modulates shark rectal gland function
Susan K. Fellner1,2,* and
Laurel Parker2
1 Department of Cell and Molecular Physiology, University of North Carolina
at Chapel Hill, Chapel Hill, NC 27599, USA
2 Mount Desert Island Biological Laboratory, Salisbury Cove, ME 04672,
USA
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Fig. 1. Cytosolic calcium [Ca2+]i response of rectal gland
artery (RGA) segments to varying concentrations of external calcium
[Ca2+]e. Each data point is part of paired observations
in which at least two concentrations of calcium were tested with each RGA
sample. Between [Ca2+]e concentrations of 0.8 and 5.3
mmol l-1, there was a linear concentration response between
[Ca2+]i and [Ca2]e
(r2=0.51, P<0.01).
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Fig. 2. Effect of L-channel blockade with nifedipine (Nif) on the response of RGA
in nominally calcium-free Ringer to the addition of external Ca2+.
Values are means ± S.E.M. Nifedipine given pre- (N=8) or post-
(N=9) calcium addition did not have any statistically significant
effect on the [Ca2+]i response. Base, baseline
value.
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Fig. 3. Cytosolic calcium [Ca2+]i response of rectal gland
artery (RGA) to external Ca2+ and Gd3+ or to spermine.
(A) Change in [Ca2+]i of RGA maintained in calcium-free
shark Ringer following the addition of Ca2+ (approx. 3 mmol
l-1) and then Gd3+ (333 µmol l-1) (values
are means ± S.E.M., N=10; *P<0.01 for
addition of Ca2+ compared to baseline [Ca2+]i
and **P<0.05 for Gd3+ compared to
Ca2+). (B) Representative example of the increase in
[Ca2+]i of RGA in calcium-free buffer in response to the
addition of spermine (333 µmol l-1) at the time indicated by the
arrow.
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Fig. 4. Representative examples of the cytosolic calcium
[Ca2+]i response of rectal gland artery (RGA) in
calcium-free buffer to the addition of external calcium, following treatment
with ryanodine (A) or with thapsigargin (TG) (B), compared to the response to
external calcium alone (C). Inhibition of sarcoplasmic reticulum
Ca2+-ATPase with TG or stimulation of the ryanodine receptor with
ryanodine raised [Ca2+]i; subsequent addition of
external Ca2+ resulted in a smaller increase in
[Ca2+]i compared to that observed in the absence of
TG.
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Fig. 5. Representative example of the effect of 2-APB (100 µmoll-1)
on cytosolic calcium levels [Ca2+]i of rectal gland
artery (RGA) to the addition of external Ca2+
[Ca2+]e. Ca2+ and 2-APB were added at the
times indicated by the arrows.
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Fig. 6. Temporal responses of grouped recordings of rectal gland artery (RGA) to
external Ca2+ and Ni2+. (A) In calcium-free medium,
Ni2+ (1 mmoll-1) promoted Ca2+ mobilization;
subsequent addition of Ca2+ (in the presence of 0.7
mmoll-1 Ni2+) further elevated cytosolic Ca2+
levels [Ca2+]i (*P< 0.01 for
Ni2+ versus baseline and Ca2+ versus
Ni2+). Values are means ± S.E.M. (N=6). (B) When
Ni2+ (1.5 mmoll-1) was added after stimulation of RGA
with external Ca2+, an inhibitory effect of Ni2+ on
Ca2+ entry was seen (representative recording). Ca2+ and
Ni2+ were added at the times indicated by the arrows.
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Fig. 7. Changes in [Ca2+]i of rectal gland tubules (RGTs) in
response to calcium, spermine and gadolinium treatment. (A) The stimulatory
effect of spermine (N=7) on [Ca2+]i in RGT was
greater than that achieved by Gd3+ (N=10)
(*P<0.01 compared to baseline,
**P<0.01 for spermine versus calcium,
 P<0.05 for Gd3+ versus
Ca2+). Values are means ± S.E.M. (B) Representative example
of the response of RGT in calcium-free shark Ringer to
[Ca2+]e followed by spermine. (C) Representative example
of RGT showing the stimulatory effect of sequential addition of external
Ca2+ and Gd3+ at the times indicated by the arrows.
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Fig. 8. Representative example of the [Ca2+]i responses of
rectal gland tubules (RGT) to thapsigargin (10-6
mmoll-1) and to the subsequent addition of external calcium (3.3
mmoll-1) added at the times indicated by the arrows.
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© The Company of Biologists Ltd 2002
