Force–velocity relationships in hypertensive arterial smooth muscle

1985 ◽  
Vol 63 (6) ◽  
pp. 669-674 ◽  
Author(s):  
C. S. Packer ◽  
N. L. Stephens
Keyword(s):  
Smooth Muscle ◽  
Spontaneously Hypertensive Rat ◽  
Peripheral Resistance ◽  
Muscle Length ◽  
Maximum Velocity ◽  
Isometric Tension ◽  
Arterial Smooth Muscle ◽  
Tension Development ◽  
Force Velocity ◽  
Wistar Kyoto

Increased total peripheral resistance is the cardinal haemodynamic disorder in essential hypertension. This could be secondary to alterations in the mechanical properties of vascular smooth muscle. Adequate study has not been made of the force–velocity (F–V) relationship in hypertensive arterial smooth muscle. Increased shortening in arterial smooth muscle would result in greater narrowing of arteries. The objectives of this investigation were to see if there is (i) increased shortening or increased maximum change in muscle length (ΔLmax where L stands for muscle length), (ii) an increased maximum velocity of shortening (Vmax) measured in lo per second where lo is the optimal muscle length for tension development, and (iii) a difference in maximum isometric tension (Po) developed in spontaneously hypertensive rat (SHR; N = 6) compared with normotensive Wistar Kyoto rat (WKY; N = 5) caudal artery strips. An electromagnetic muscle lever was employed in recording force–velocity data. Analysis of these data revealed the following: (a) the SHR mean Po of 6.21 ± 1.01 N/cm2 was not different from the mean WKY Po of 6.97 ± 1.64 N/cm2 (p > 0.05); (b) the SHR preparations showed greater shortening for all loads imposed; (c) the SHR Vmax of 0.016 lo/s was greater than the WKY Vmax of 0.013 lo/s (p < 0.05). This study provides evidence that while hypertensive arterial smooth muscle is not able to produce more force than normotensive arterial smooth muscle, it is capable of faster and greater shortening. The latter could result in increased narrowing of hypertensive arteries and increased blood pressure.

Tension–velocity relationships in hypertensive mesenteric resistance arteries

1985 ◽  
Vol 63 (6) ◽  
pp. 675-680 ◽  
Author(s):  
C. S. Packer ◽  
N. L. Stephens
Keyword(s):  
Smooth Muscle ◽  
Enzyme Inhibitor ◽  
Spontaneously Hypertensive Rat ◽  
Peripheral Resistance ◽  
Maximum Velocity ◽  
Arterial Smooth Muscle ◽  
Tension Development ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat ◽  
Wistar Kyoto

Increased total peripheral resistance is the cardinal haemodynamic disorder in essential hypertension. This could be secondary to alterations in the mechanical properties of vascular smooth muscle. Adequate study has not been made of the tension–velocity (T–V) relationship in hypertensive resistance arterial smooth muscle. Increased narrowing in such arteries would result in increased resistance. The objectives of this investigation were to determine whether there is (i) increased narrowing capacity (−ΔC/Co where C stands for arterial internal circumference and Co is the optimal arterial internal circumference for maximum tension development); (ii) an increased maximum velocity of isobaric narrowing (Vmax) measured in Co per second; (iii) an increased wall thickness (h); and (iv) an increased active stress development (Tmax) in the spontaneously hypertensive rat (SHR; n = 5) compared with the normotensive Wistar Kyoto (WKY; n = 5) and MK-421 (an angiotensin I converting enzyme inhibitor) treated spontaneously hypertensive rat (MK-421 trt. SHR; n = 5) mesenteric resistance (diameter, < 300 μm) arteries. Analysis of the data for arteries constricting isobarically against a range of pressures revealed that (a) the SHR–ΔC/Co values at pressures ranging from 20 to 120 mmHg (1 mmHg = 133.322 Pa) showed significantly increased narrowing compared with the MK-421 trt. SHR and WKY–ΔC/Co values in this same pressure range (p < 0.01), and (b) the SHR derived Vmax of 0.83 ± 0.08 Co/s was significantly faster than either the MK-421 trt. SHR or WKY Vmax of 0.34 ± 0.06 and 0.28 ± 0.08 Co/s, respectively (p < 0.01); (c) the SHR mean h of 31 ± 3 μm was significantly thicker than either the MK-421 trt. SHR or WKY arteries of 22 ± 2 and 19.5 ± 0.5μm, respectively (p < 0.05); (d) the SHR, MK-421 trt. SHR, and WKY arteries showed no differences in Tmax which were 1016 ± 135, 897 ± 221, and 1077 ± 43 g/cm2, respectively (p > 0.05). This study provides evidence that while the hypertensive resistance arterial segments are not able to produce more tension than normotensive arterial smooth muscle, they are able to narrow faster and narrow more. The latter would result in increased resistance and could result in increased blood pressure.

Stiffness of active smooth muscle during forced elongation

1987 ◽  
Vol 253 (3) ◽  
pp. C484-C493 ◽  
Author(s):  
R. A. Meiss
Keyword(s):  
Smooth Muscle ◽  
Phase Angle ◽  
Muscle Length ◽  
Isometric Tension ◽  
Microcomputer System ◽  
Tension Development ◽  
Stretch Rate ◽  
Angle Data ◽  
Cross Bridges ◽  
System Phase

The stiffness of isometrically contracting mesotubarium superius and ovarian ligament smooth muscle from estrous female rabbits was measured continuously by using sinusoidal length perturbations (at 80 Hz, less than 15 microns peak to peak). Muscles were stimulated with alternating current fields, and all records were digitized using a microcomputer system. Phase-angle data were used to resolve computed stiffness into elastic and viscous components. Stiffness measurements were continued during long ramp-type stretches (up to 25% of muscle length) delivered as soon as force was maximal. To use the period of isometric tension development as a standard for comparison, the expected stiffness was computed during the long stretch. Stiffness was reduced in approximate proportion to the ramp stretch rate, and the reduction was confined largely to the elastic component. Cooling the muscle increased the stiffness deviation at a given stretch rate. It is proposed that the long stretch detaches cross bridges that can reattach to new sites as myofilaments shear past one another. At higher shearing speeds, less time is available for reattachment and stiffness is further reduced.

An abnormal rate of actin myosin cross-bridge cycling in colonic smooth muscle associated with experimental colitis

1992 ◽  
Vol 262 (5) ◽  
pp. G921-G926 ◽  
Author(s):  
Y. N. Xie ◽  
W. T. Gerthoffer ◽  
S. N. Reddy ◽  
F. Cominelli ◽  
V. E. Eysselein ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Maximum Velocity ◽  
Experimental Colitis ◽  
Smooth Muscle Contraction ◽  
Isometric Tension ◽  
Mucosal Inflammation ◽  
Control Group ◽  
Tension Development ◽  
Abnormal Rate ◽  
Mlc Phosphorylation

Previous studies showed that colonic smooth muscle develops less contractile force to neurohumoral stimulation when associated with mucosal inflammation. This study evaluated 1) the Ca2+ dependence for colonic smooth muscle contraction, 2) the maximum velocity of muscle shortening (Vmax), and 3) changes in 20-kDa myosin light-chain (MLC) phosphorylation in distal circular colonic muscle from healthy rabbits and from rabbits with experimental colitis, induced by Formalin and immune complexes. The isometric tension of unskinned muscle stimulated with bethanechol or KCl was less (P less than 0.05) in animals with colitis compared with the control group. In saponin-skinned muscle, the amplitude of the maximal tension at [Ca2+] of 3 x 10(-7) M was decreased (P less than 0.05) in colitis animals (4.3 +/- 0.9 x 10(4) N/m2, n = 7) compared with healthy animals (10.5 +/- 2.4 x 10(4) N/m2, n = 6). However, the ED50 for Ca2+ stimulation was similar (P greater than 0.05) in both groups. When MLC was thiophosphorylated with ATP gamma S, the tension development was decreased in colitis (2.1 +/- 0.3 x 10(4) N/m2, n = 5; P less than 0.01) compared with normals (5.0 +/- 1.4 x 10(4) N/m2, n = 5). In healthy animals, phosphorylation of 20-kDa MLC increased rapidly to 51.2 +/- 3.1% within 15 s after stimulation and subsequently declined to 19.0 +/- 2.1% at 5 min. Vmax was maximal (0.14 Lo/s) 13 s after stimulation and declined before maximal active isometric stress. In colitis animals, the 20-kDa MLC phosphorylation (P less than 0.05) and the Vmax (P less than 0.01) were decreased.(ABSTRACT TRUNCATED AT 250 WORDS)

Decreased velocity of shortening in arterial smooth muscle from older (28- to 31-week-old) spontaneously hypertensive rats

1986 ◽  
Vol 64 (1) ◽  
pp. 96-100 ◽  
Author(s):  
C. S. Packer ◽  
M. L. Kagan ◽  
N. L. Stephens
Keyword(s):  
Smooth Muscle ◽  
Spontaneously Hypertensive Rats ◽  
Maximum Velocity ◽  
Hypertensive Rats ◽  
Arterial Smooth Muscle ◽  
Spontaneously Hypertensive ◽  
Velocity Of Shortening ◽  
Old Rats ◽  
Force Velocity ◽  
Arterial Muscle

An increased maximum velocity of shortening (Vmax) and increased shortening ability (ΔLmax) have been reported for caudal arterial smooth muscle from 16- to 18-week-old spontaneously hypertensive rats (SHR) compared with age-matched Wistar-Kyoto (WKY) control rats. It is known that hypertension results in hypertrophy of vascular smooth muscle. It is plausible that the faster Vmax of 16- to 18-week-old SHR arterial smooth muscle may slow down with age due to hypertrophy. The force–velocity (F–V) study done previously on caudal arterial strips from 16- to 18-week-old SHR and WKY rats was repeated on preparations from 28- to 31-week-old rats. An electromagnetic muscle lever was employed in recording force–velocity data. Analysis of these data revealed that the 28- to 31-week-old SHR (n = 7) mean F–V curve was not different from the 28- to 31-week-old WKY (n = 5) mean F–V curve (p > 0.05), and the shortening ability of 28- to 31-week-old SHR arterial muscle was significantly depressed compared with 28- to 31-week-old WKY arterial muscle (p < 0.01). In conclusion, (i) although Vmax is faster in younger (16- to 18-week-old) SHR compared with age-matched WKY caudal arterial smooth muscle, SHR Vmax is not different from WKY Vmax in the older (28- to 31-week-old) rats, (ii) Shortening ability is greater in 16- to 18-week-old SHR caudal arterial strips compared with 16- to 18-week-old WKY strips, but is significantly depressed in 28- to 31-week-old SHR compared with 28- to 31-week-old WKY preparations. It can also be concluded that the decrease in SHR Vmax from once elevated speeds is not due simply to ageing, for if this were the case, the WKY Vmax should also decline with age and the relative difference between SHR and WKY F–V curves seen in younger rats should not have been obliterated when comparing the older rats.

Force–velocity constants in smooth muscle: afterloaded isotonic and quick-release methods

1985 ◽  
Vol 63 (1) ◽  
pp. 48-51 ◽  
Author(s):  
N. L. Stephens
Keyword(s):  
Smooth Muscle ◽  
Muscle Length ◽  
Maximum Velocity ◽  
Electrical Stimulus ◽  
Active State ◽  
Quick Release ◽  
Velocity Of Shortening ◽  
Force Velocity ◽  
Release Method ◽  
Tetanic Tension

In using pharmacologic stimuli, force–velocity (FV) curves are usually obtained by the method of quick release (QR) and redevelopment of shortening at peak tetanic tension; the advantage of the method being that the active state is at maximum. However, the QR may itself reduce the intensity of the active state and result in reduced values of FV constants. We tested this by delineating FV curves in canine tracheal smooth muscle using both conventional afterloaded isotonic contractions (ALI), and redevelopment of shortening after QR methods. For both these studies a supramaximal tetanizing electrical stimulus was used. The analysis of 11 experiments revealed that the latter method resulted in statistically significant reductions of all FV constants except for Po (maximum isometric tetanic tension). The means and standard errors for the sets of constants for the ALI and QR, respectively, are as follows: Vmax (maximum velocity of shortening) = 0.275 lo (optimal muscle length)/s ± 0.024 (SE), and 0.216 lo/s + 0.023; a (hyperbolic constant with units of force) = 294 g/cm2 ± 35 and 236 g/cm2 ± 32; b (hyperbolic constant with units of velocity) = 0.059 lo ± 0.004 and 0.039 lo/s ± 0.005; a/Po = 0.214 ± 0.028 and 0.182 ± 0.026; and Po = 1.362 kg/cm2 ± 0.106 and 1.294 kg/cm2 ± 0.097. These data clearly show that the quick-release method for measuring force–velocity relationships in canine smooth muscle results in significant underestimates of muscle shortening properties.

scholarly journals Rate-limiting steps in the tension development of freeze-glycerinated vascular smooth muscle.

1982 ◽  
Vol 79 (3) ◽  
pp. 437-452 ◽  
Author(s):  
J W Peterson
Keyword(s):  
Smooth Muscle ◽  
Protein Content ◽  
Time Course ◽  
Isometric Tension ◽  
Native Protein ◽  
Arterial Smooth Muscle ◽  
Tension Development ◽  
Rate Limiting Step ◽  
Limiting Step ◽  
Rate Limiting

A method for "skinning" arterial smooth muscle is presented which yields isometric tension development typically 60-80% of maximum physiological tension in the presence of micromolar Ca++ and millimolar Mg-ATP, while retaining essentially the native protein content. Using the methods of "CA jump," the time-course of Ca++-activated tension development in the skinned artery can be made identical to, but not faster than, the rate of tension development in the intact artery. In the skinned artery, activating free [Ca++] does not substantially alter the rate at which tension development approaches the final steady tension attained at that free [Ca++] (less than 25% decline in speed for a 10-fold decrease in [Ca++]). These observations are taken to mean that the rate-limiting step in isometric tension development in arterial smooth muscle does not depend directly on Ca++.

Active Contractions of Ureteral Segments

1985 ◽  
Vol 107 (1) ◽  
pp. 62-67 ◽  
Author(s):  
P. F. Zupkas ◽  
Y. C. Fung
Keyword(s):  
Constitutive Equation ◽  
Isometric Contraction ◽  
Smooth Muscles ◽  
Muscle Length ◽  
Maximum Velocity ◽  
Fixed Time ◽  
Tension Development ◽  
Force Velocity ◽  
Contraction Cycle

The first step in the analysis of the biomechanics of any organ is to obtain its constitutive equation. In pursuit of a constitutive equation describing the peristalsis of the ureter, we measured the relationship between the length of the muscle, the velocity of contraction, and the active tension development of isolated ureter segments. The results of length-tension measurements (giving the maximum tension developed in isometric contraction of a ureter segment of specific length) were similar to those obtained by previous investigators and reflected the behavior of length-tension relationships for other smooth muscles. Two aspects of the force-velocity relationship of the ureter were examined: the effect of releasing the ureter at different times after stimulation, and that at different levels of afterload. Measurements were analyzed using the hyperbolic Hill’s equation in the form T/T0=(1−v/v0)(1+cv/v0)−1 where v is the velocity of contraction, v0 is the velocity of contraction when T = 0, T is the tension in the muscle after release, T0 is the tension in the muscle immediately prior to c is the dimensionless constant. The results of force-velocity measurements showed that the so-called “maximum” velocity v0, is the largest if the tension is released at a time of contraction, early in the rise portion of the contraction cycle. Further, if tension is released from an isometric contraction at a fixed time in the rise portion of the contraction cycle, the largest value of v0 is obtained when the muscle length is in the range of 0.85–0.90 Lmax. Interestingly, the in vivo length of the ureter lies also in this range, 0.85–0.90 Lmax.

Muscle shortening increases sensitivity of fatigue to severe hypoxia in canine diaphragm

1991 ◽  
Vol 71 (6) ◽  
pp. 2309-2316 ◽  
Author(s):  
B. T. Ameredes ◽  
M. W. Julian ◽  
T. L. Clanton
Keyword(s):  
Flow Characteristics ◽  
Muscle Length ◽  
Isometric Tension ◽  
Severe Hypoxia ◽  
Mean Power ◽  
Tension Development ◽  
Moderate Hypoxia ◽  
O2 Supply ◽  
Mean Power Output

The effects of inspired O2 on diaphragm tension development during fatigue were assessed using isovelocity (n = 6) and isometric (n = 6) muscle contractions performed during a series of exposures to moderate hypoxia [fraction of inspired O2 (FIO2) = 0.13], hyperoxia (FIO2 = 1), and severe hypoxia (FIO2 = 0.09). Muscle strips were created in situ from the canine diaphragm, attached to a linear ergometer, and electrically stimulated (30 Hz) to contract (contraction = 1.5 s/relaxation = 2 s) from optimal muscle length (Lo = 8.9 cm). Isovelocity contractions shortened to 0.70 Lo, resulting in a mean power output of 210 mW/cm2. Fatigue trials of 35 min duration were performed while inspired O2 was sequentially changed between the experimental mixtures and normoxia (FIO2 = 0.21) for 5-min periods. In this series, severe hypoxia consistently decreased isovelocity tension development by an average of 0.1 kg/cm2 (P less than 0.05), which was followed by a recovery of tension (P less than 0.05) on return to normoxia. These responses were not consistently observed in isometric trials. Neither isovelocity nor isometric tension development was influenced by moderate hypoxia or hyperoxia. These results demonstrate that the in situ diaphragm is relatively insensitive to rapid changes in O2 supply over a broad range and that the tension development of the shortening diaphragm appears to be more susceptible to severe hypoxia during fatigue. This may reflect a difference in either the metabolic or blood flow characteristics of shortening contractions of the diaphragm.

Induction of a myogenic response in tonic airway smooth muscle by tetraethylammonium

1975 ◽  
Vol 228 (2) ◽  
pp. 628-632 ◽  
Author(s):  
NL Stephens ◽  
EA Kroeger ◽  
U Kromer
Keyword(s):  
Smooth Muscle ◽  
Muscle Length ◽  
Maximum Velocity ◽  
Threshold Concentration ◽  
Myogenic Response ◽  
Experimental Conditions ◽  
Tetraethylammonium Chloride ◽  
High K ◽  
Increase Membrane Permeability ◽  
Ionic Basis

In multi-unit tracheal smooth muscle (TSM), quick stretches applied at a velocity of 5 times the measured maximum velocity of isotonic shortening of the muscle, of a magnitude 3 times the measured extension of the series-elastic component when the muscle contracts maximally, and at optimal muscle length (L-o) were unable to elicit any myogenic response (MR). Experimental conditions such as hypoxia (P-O2 smaller than 60 mmHg) and acidosis (pH equals 6.8) or the presence of Ba2+ (2 mM), acetylcholine (10-6 M), or high (K+)-o (59 mM) were also unable to elicit the MR. However, tetraethylammonium chloride (TEA, 0.4-67 mM) produces 1) spontaneous phasic contractions and 2) a MR to quick stretch. The ionic basis for these changes was then investigated by studying the Ca and Mg dependence of the response to TEA. The dose-response relationship to TEA was shifted to the left by decreasing external Mg2+ from 2.5 to 0.5 mM. The ability of TSM to produce a MR was absolutely dependent on external Ca, but the threshold concentration required shifted from 2.5 times 10-5 M at normal external Mg (2.5 mM) to 5 times 10-4 M at the reduced external Mg (0.5 mM). The effects of TEA on spontaneity and the MR were abolished by D-600. These results suggest that 1) TEA functionally converts multiunit smooth muscle into a single unit one and leads to the development of a MR and 2) the MR results from a depolarization-activated mobilization of Ca and is inhibited by ionic conditions known to increase membrane permeability.

scholarly journals Series-to-parallel transition in the filament lattice of airway smooth muscle

2000 ◽  
Vol 89 (3) ◽  
pp. 869-876 ◽  
Author(s):  
Chun Y. Seow ◽  
Victor R. Pratusevich ◽  
Lincoln E. Ford
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Muscle Length ◽  
Thick Filament ◽  
Cycling Rate ◽  
Cross Bridge ◽  
Parallel Change ◽  
Force Velocity ◽  
Cross Bridges ◽  
Trachealis Muscle

Force-velocity curves measured at different times during tetani of sheep trachealis muscle were analyzed to assess whether velocity slowing could be explained by thick-filament lengthening. Such lengthening increases force by placing more cross bridges in parallel on longer filaments and decreases velocity by reducing the number of filaments spanning muscle length. From 2 s after the onset of stimulation, when force had achieved 42% of it final value, to 28 s, when force had been at its tetanic plateau for ∼15 s, velocity decreases were exactly matched by force increases when force was adjusted for changes in activation, as assessed from the maximum power value in the force-velocity curves. A twofold change in velocity could be quantitatively explained by a series-to-parallel change in the filament lattice without any need to postulate a change in cross-bridge cycling rate.

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