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First published online February 15, 2008
Journal of Experimental Biology 211, 766-772 (2008)
Published by The Company of Biologists 2008
doi: 10.1242/jeb.007658
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Elasticity, unexpected contractility and the identification of actin and myosin in lobster arteries

J. L. Wilkens1,*, M. J. Cavey1, I. Shovkivska2, M. L. Zhang2 and H. E. D. J. ter Keurs2

1 Department of Biological Sciences, Faculty of Science, University of Calgary, 2500 University Drive N.W., Calgary, Alberta, T2N 1N4, Canada
2 Department of Physiology and Biophysics, Faculty of Medicine, University of Calgary, 4440 Hospital Drive N.W., Calgary, Alberta, T2N 4N1, Canada


Figure 1
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  		Fig. 1. Sternal artery. (A) Arterial spread treated with Rhodamine–phalloidin. Staining of the cells in the middle layer (tunica intermedia) of the vessel is strong. Scale bar, 100 µm. (B) Horizontal electron micrograph of an artery where the inner layer (ti, tunica interna) interfaces with the tunica intermedia. Bundles of microfilaments (mf) appear in the cortical cytoplasm and account for the fluorescence of cells in the tunica intermedia. Individual microfilaments are ~6.5 nm in diameter. Dense filamentous mats are applied to the inner and outer surfaces of the plasmalemmata. Scale bar, 1 µm.

 

Figure 2
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  		Fig. 2. SDS-PAGE of three arteries (ALA, SA and DAA), the ostial muscle (OOM), and the slow and fast skeletal muscles, shows bands identified as actin, myosin and tropomyosin. The left-hand lane (MW) contains protein markers of known molecular mass (in kDa). Labelled on the right are myosin heavy chain (MHC), paramyosin (P1, 2), P75 in fast skeletal muscle, actin, tropomyosin (Tm), and troponins T (TnT) and I (Tnl).

 

Figure 3
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  		Fig. 3. Stress–strain plots of three arteries. Strain was obtained by dividing the increments of stretch, {Delta}l, by the unstretched circumference, Lo. For stress (kPa), the passive force (in mN) is divided by the cross-sectional wall area (longitudinal ring width multiplied by wall thickness).

 

Figure 4
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  		Fig. 4. (A) Response of a hepatic artery (HA) ring to continuous superfusion with glutamic acid (GLU; 10 mmol l–1). Wall force at the time of GLU application was 0.170 mN. (B) Response of a sternal artery (SA) ring, at an initial wall force of 0.914 mN, to continuous superfusion with proctolin (PR; 1.0 µmol l–1).

 

Figure 5
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  		Fig. 5. Contraction of a dorsal abdominal artery (DAA) ring in response to (A) electrical stimulation (bar, 5 ms pulses, 20 Hz, 5 s duration) and (B,C) continuous superfusion with (B) glutamic acid (GLU; 10 mmol l–1) and (C) proctolin (PR; 1.0 µmol l–1).

 

Figure 6
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  		Fig. 6. Force–extension relationships for anterior lateral artery (ALA), sternal artery (SA) and dorsal abdominal artery (DAA) rings. The response to gradual stretch was determined first. Then, the length was reduced from maximum stretch to the test length where PR (proctolin; squares) or glutamic acid (GLU; triangles) was applied. The DAA response to PR is almost buried in the curve. The amount that the drug-induced contraction would have shortened the ring if it were free to move was determined as shown for the SA.

 

Figure 7
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  		Fig. 7. Effect of cytochalasin D (CD; 0.5 µg ml–1) pretreatment on a sternal artery (SA) ring and an ostial muscle (OOM). (A) Contraction of an SA ring in response to continuous perfusion with proctolin (PR; 1.0 µmol l–1). (B) Effect of CD pretreatment on a PR-induced contraction in an adjacent SA ring. (C) Effect of CD (2.5 min) on basal tonus and electrically stimulated tetanic contractions of an OOM.

 

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© The Company of Biologists Ltd 2008