The kinetics of post-vibration tension recovery of the isolated rat portal vein.

1. The kinetics of post-vibration tension recovery have been examined during electrical, noradrenaline or KCl stimulation of the isolated rat portal vein. 2. Inhibition of isometric contractions produced by a combination of noradrenaline (20 microM) and KCl (53 mM) by longitudinal, 100 Hz sinusoidal vibration increased with increasing vibration amplitude up to a maximum of 78.7% of the active tension. This inhibition was little affected by a decrease in temperature from 37 to 25 degrees C. Recovery of tension after the end of vibration was complete and took place exponentially. The time constant for this recovery was little affected by changes in vibration amplitude, but increased from 1.72 +/- 0.09 to 4.35 +/- 0.33 sec, for large amplitude vibrations, when the temperature was lowered from 37 to 25 degrees C. 3. The increase in isometric tension during 50 Hz a.c. electrical field stimulation was exponential, apart from a minor initial activation component, and took place with a time constant of 1.25 +/- 0.17 sec. Neither delaying nor interrupting development of this contraction with inhibitory vibration altered the time constant for this exponential increase in tension. There was no correlation between the time constant and the maximum active tension achieved after vibration was stopped. 4. Post-vibration tension recovery during electrical, noradrenaline (20 microM) or KCl (120-130 mM) stimulation was independent of the nature of the stimulus at comparable times of stimulation, but the time constant increased during exposures of more than 10 sec to either noradrenaline or KCl. With noradrenaline, the increase was from 1.45 +/- 0.10 sec after 50 sec of stimulation to 2.24 +/- 0.16 sec after 336 sec of stimulation (P less than 0.0005). Such an increase in the time constant may reflect slower cycling of cross-bridges with an improvement in the efficiency by which contraction is maintained. 5. The kinetics of post-vibration tension recovery were those of a monomolecular or, as is more likely, a pseudo-monomolecular chemical reaction. A cross-bridge attachment model based on such a reaction has been used to interpret the observations.

The temperature dependence of parallel and series elastic elements in the vascular smooth muscle of the rat portal vein.

The stiffness of a parallel (PE) as well as of a series elastic element (SE) in the isolated rat portal vein was determined at 37 degrees C and at 25 degrees C. The length-tension curve of the PE was obtained by a stepwise lengthening of the preparation and showed no temperature dependence for the element: the mean extension of the PE was 48.8% of the optimum length L0 at 37 degrees C, and 47.3% of L0 at 25 degrees C when loaded with the maximum active force T0. The maximum force occurred at both temperatures with the same muscle length. Even the stiffness factor, i.e. the slope 'k' of the linear function dT/dL = k . T + c showed no temperature dependence. The series elasticity was determined by means of the quick-release technique from afterloaded isometric contractions of the tetanized preparation. A distinct temperature influence was revealed by the decrease of the mean SE extension from 13.5% of L0 at 37 degrees C to 10.9% of L0 at 25 degrees C (P less than 0.0005). The stiffness factor, normalized to the actual muscle length, was 12.0 per ML at 37 degrees C and 14.7 per ML at 25 degrees C (P less than 0.025). The values obtained for the portal vein are equivalent to those calculated for other smooth muscle preparations but the stiffness of series elasticity is well below that found in the cardiac and skeletal muscle.