Active tension adaptation at a shortened arterial muscle length: inhibition by cytochalasin-D.
Unlike the static length-tension curve of striated muscle, airway and urinary bladder smooth muscles display a dynamic length-tension curve. Much less is known about the plasticity of the length-tension curve of vascular smooth muscle. The present study demonstrates that there were significant increases of ∼15% in the phasic phase and ∼10% in the tonic phase of a third KCl-induced contraction of a rabbit femoral artery ring relative to the first contraction after a 20% decrease in length from an optimal muscle length (L(0)) to 0.8-fold L(0). Typically, three repeated contractions were necessary for full length adaptation to occur. The tonic phase of a third KCl-induced contraction was increased by ∼50% after the release of tissues from 1.25-fold to 0.75-fold L(o). The mechanism for this phenomenon did not appear to lie in thick filament regulation because there was no increase in myosin light chain (MLC) phosphorylation to support the increase in tension nor was length adaptation abolished when Ca(2+) entry was limited by nifedipine and when Rho kinase (ROCK) was blocked by H-1152. However, length adaptation of both the phasic and tonic phases was abolished when actin polymerization was inhibited through blockade of the plus end of actin by cytochalasin-D. Interestingly, inhibition of actin polymerization when G-actin monomers were sequestered by latrunculin-B increased the phasic phase and had no effect on the tonic phase of contraction during length adaptation. These data suggest that for a given level of cytosolic free Ca(2+), active tension in the femoral artery can be sensitized not only by regulation of MLC phosphatase via ROCK and protein kinase C, as has been reported by others, but also by a nonmyosin regulatory mechanism involving actin polymerization. Dysregulation of this form of active tension modulation may provide insight into alterations of large artery stiffness in hypertension.
Departments of Physiology, School of Engineering, Virginia Commonwealth University, Richmond, 23298-0614, USA. mbednarek@chatham.edu
Melissa L
ML
Bednarek
John E
JE
Speich
Amy S
AS
Miner
Paul H
PH
Ratz
D019307:1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine / Q000031:analogs & derivatives / Q000494:pharmacology; D000199:Actins / Q000187:drug effects / Q000378:metabolism; D000818:Animals; D019086:Bridged Bicyclo Compounds, Heterocyclic / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000187:drug effects / Q000502:physiology; D015638:Cytochalasin D / Q000494:pharmacology*; D005263:Femoral Artery / Q000187:drug effects*; D009119:Muscle Contraction / Q000187:drug effects* / Q000502:physiology; D009129:Muscle Tonus / Q000187:drug effects / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000187:drug effects* / Q000502:physiology; D018994:Myosin Light Chains / Q000378:metabolism / Q000502:physiology; D009543:Nifedipine / Q000494:pharmacology; D010766:Phosphorylation; D011189:Potassium Chloride / Q000494:pharmacology; D011817:Rabbits; D053778:Thiazolidines / Q000494:pharmacology; D054460:rho-Associated Kinases / Q000037:antagonists & inhibitors
C459092:2-methyl-1-((4-methyl-5-isoquinolinyl)sulfonyl)homopiperazine; D000199:Actins; D019086:Bridged Bicyclo Compounds, Heterocyclic; D002121:Calcium Channel Blockers; D015220:Calcium Channels; D018994:Myosin Light Chains; D053778:Thiazolidines; D015638:Cytochalasin D; D011189:Potassium Chloride; D019307:1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; D054460:rho-Associated Kinases; D009543:Nifedipine; C037068:latrunculin B
Am J Physiol. 1981 Oct;241(4):H557-63
7315980
Am J Physiol. 1995 Jun;268(6 Pt 1):C1332-41
7611350
Am J Physiol. 1989 Jan;256(1 Pt 1):C96-100
2463763
Circ Res. 1973 Sep;33(3):275-83
4746719
J Muscle Res Cell Motil. 1999 Jan;20(1):11-8
10360230
J Appl Physiol (1985). 2006 Oct;101(4):1189-98
16778004
Trends Biochem Sci. 2006 Apr;31(4):197-205
16542844
Can J Physiol Pharmacol. 2005 Oct;83(10):841-50
16333355
J Muscle Res Cell Motil. 1992 Apr;13(2):206-18
1534566
Pharmacol Rev. 1968 Dec;20(4):197-272
4888390
Am J Physiol Cell Physiol. 2003 Dec;285(6):C1377-85
12890649
Cardiovasc Res. 2009 Feb 15;81(3):439-48
18974044
Hypertension. 2009 Aug;54(2):375-83
19564542
Am J Physiol Cell Physiol. 2006 Jun;290(6):C1552-9
16421202
Circ Res. 1990 May;66(5):1354-61
2335031
Am J Physiol Cell Physiol. 2005 Jul;289(1):C12-21
15716326
Mol Cell Biochem. 2003 Jun;248(1-2):105-14
12870661
Am J Physiol Cell Physiol. 2008 Sep;295(3):C576-87
18596210
J Cell Sci. 2005 Jun 1;118(Pt 11):2381-92
15923651
Can J Physiol Pharmacol. 1994 Nov;72(11):1400-9
7767885
Am J Physiol Cell Physiol. 2008 Sep;295(3):C768-78
18596213
Respir Physiol Neurobiol. 2003 Sep 16;137(2-3):151-68
14516723
Cell Calcium. 2009 Jul;46(1):65-72
19487023
IEEE Eng Med Biol Mag. 2007 Jan-Feb;26(1):62-70
17278774
J Muscle Res Cell Motil. 2004;25(1):7-19
15160483
FASEB J. 1987 Sep;1(3):177-85
3040504
J Smooth Muscle Res. 1996 Apr;32(2):51-60
8845566
J Appl Physiol (1985). 2000 Nov;89(5):2065-72
11053363
Curr Hypertens Rep. 2009 Jun;11(3):190-6
19442328
Acta Physiol Scand. 1976 Mar;97(1):1-12
818878
Am J Physiol Renal Physiol. 2009 Oct;297(4):F1119-28
19675182
J Gen Physiol. 1979 Jul;74(1):85-104
479823
J Physiol. 1995 Nov 1;488 ( Pt 3):729-39
8576862
Am J Physiol. 1971 Nov;221(5):1243-9
5124267
J Cell Biol. 1972 Jan;52(1):105-16
4621356
Hypertension. 1995 Jul;26(1):48-54
7607732
J Physiol. 1960 Nov;154(1):15-25
16992066
J Appl Physiol (1985). 2004 Dec;97(6):2029-34
15531570
J Pharmacol Exp Ther. 2009 Feb;328(2):399-408
19011165
J Appl Physiol (1985). 2007 May;102(5):1746-55
17234807
Circ Res. 1993 Jun;72(6):1308-16
8388324
Am J Physiol. 1995 Aug;269(2 Pt 1):C417-23
7653524
J Appl Physiol (1985). 2008 Apr;104(4):1014-20
18218913
J Cell Biol. 1977 Dec;75(3):990-6
562890
J Physiol. 1974 Nov;243(1):1-43
4449057
Clin Exp Pharmacol Physiol. 2007 Jul;34(7):647-51
17581224
Am J Physiol. 1994 Oct;267(4 Pt 2):H1437-46
7943389
Arch Int Pharmacodyn Ther. 1974 Jul;210(1):67-74
4441184