First published online February 4, 2005
Journal of Experimental Biology 208, 737-747 (2005)
Published by The Company of Biologists 2005
doi: 10.1242/jeb.01430
Sites and modes of action of proctolin and the FLP F2 on lobster cardiac muscle
J. L. Wilkens1,*,
T. Shinozaki2,
T. Yazawa3 and
H. E. D. J. ter Keurs4
1 Department of Biological Sciences, University of Calgary, Calgary,
Canada
2 Department of Cardiovascular Medicine, Tohoku Graduate School of Medical
Sciences, Sendai, Japan
3 Department of Biology, Tokyo Metropolitan University, Minamiohsawa 1-1,
Hachioji, Japan
4 Faculty of Medicine, University of Calgary, Calgary, Canada
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Fig. 1. The effects of proctolin, F2 and glutamic acid on force
development of lobster cardiac ostia. In (A) and (B) the threshold
concentration of each peptide was continuously perfused for 4 min, in the
other four traces (C-F) the peptide or glutamic acid (Glu) was present for 30
s. Tetani were produced by trains of stimuli (5 ms pulses, 20 Hz, 200 ms train
duration, 2 trains min-1).
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Fig. 8. (A) Potentiation of tetani produced by prolonged electrical stimulation
with 2 ms stimuli, 50 Hz for 3.5 s. The single tetani before and following
prolonged stimulation were produced by 2 ms stimuli, 50 Hz and 200 ms train
duration. Caffeine-induced contractures (arrows, 1 mmol l-1 for 30
s) applied before and following a (B) proctolin (1 µmol l-1 for
30 s) and a (C) F2 (1 µmol l-1 for 30 s) induced
contracture. (D) Caffeine pulses (arrows, 10 mmol l-1 for 60 s)
applied before and following a glutamic acid pulse (10 mmol l-1 for
60 s). There were no electrical stimuli delivered during PR-, F2-
and Glu-induced contractures.
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Fig. 2. (A) Effect of PR (1 µmol l-1, 90 s) on membrane potential
(mV) and input resistance (uncalibrated, downward deflections, upper trace),
and on tetani and contracture (lower trace). The resting membrane potential
before PR was -68 mV. During the contracture there was a period of 2 min
during which the OOM showed oscillations in membrane potential and force. (B)
Effect of F2 (1 µmol l-1, 90 s) on membrane potential
(mV) and input resistance (uncalibrated, downward deflections, upper trace),
and on tetani and contracture (lower trace). The resting membrane potential
before F2 was -80 mV. During the contracture there were spontaneous
contractions and fluctuations in membrane potential.
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Fig. 3. Normalized augmentation of tetani following pulses of PR or F2
(0.1 µmol l-1, 30 s) for OOM equilibrated in normal and reduced
[Ca2+]o (2, 6 and 18 mmol l-1, respectively;
N=4; *P<0.05).
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Fig. 4. The [Ca2+]i and force of an OOM during exposure to
three concentrations of proctolin. The peptide was applied for 60 s. Time zero
is a response before peptide arrival, the other numbers written above the
tetani are time in minutes after PR. The tetani were produced by trains of
stimuli (1 ms pulses, 30 Hz, 300 ms train duration, 0.1 trains
s-1).
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Fig. 5. Force/intracellular pCa loops taken before (time=0) and at various times in
minutes after a 60 s exposure to 1 µmol l-1 proctolin. Each loop
represents a tetanus produced by a stimulus train (as in
Fig. 4). The elevated force
during the diastolic period represents the period of contracture. The
arrowhead on the zero time trace shows the direction of the changes in force
and pCa.
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Fig. 6. Effects of L-type voltage-gated Ca2+ channel blockers on
responses to proctolin and F2. (A) OOM was perfused with nifedipine
(0.1 mmol l-1) saline for 30 min before 30 s pulses of PR and
F2 (0.1 µmol l-1 each). (B) Verapamil (0.1 mmol
l-1) was perfused for 31 min before 30 s pulses of PR and
F2 (0.1 µmol l-1 each). (C) CdCl2 (1 mmol
l-1) greatly attenuated tetani, but did not prevent contractures
following 30 s pulses of PR (0.1 µmol l-1) or F2 (10
nmol l-1).
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Fig. 7. Na+-free saline greatly attenuated tetani and caused a
contracture. At the points indicated by arrows PR and F2 (0.1
µmol l-1 each, 30 s) caused small contractures.
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Fig. 9. Continuous perfusion with caffeine saline (10 mmol l-1) reduced
or eliminated tetani, but had little effect on basal tonus. In both traces the
peptide-induced contracture developed more rapidly and was greater in
amplitude during the period of caffeine exposure then before. The recovery of
the contracture was faster than in the absence of caffeine. Note the rapid
recovery of tetani immediately following the washout of caffeine in (B).
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Fig. 10. Effect of ryanodine (10 µmol l-1) on the
[Ca2+]i and force responses of an OOM to two
concentrations of proctolin (10 nmol l-1 and 1 µmol
l-1). The OOM had been superfused with saline-containing ryanodine
for a minimum of 30 min before the peptide challenges. Stimulus trains
consisted of 1 ms pulses, 50 Hz, 500 ms train duration, 0.1 trains
s-1.
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© The Company of Biologists Ltd 2005
