[Possible significance of prostaglandins for human vascular motility and hypertension].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to R Laven.
Explore the source record for details and available documents.
The kinetics of vascular smooth musclw activity was studied by means of afterloaded isotonic contractions of the tetanized rat portal vein at varied pH (8.0-5.9), pCa (3.4-2.1), and during noradrenaline incubation (0.4 mug/ml). Under control conditions (pH 7.3, pCa 2.6) the following parameters of the force velocity relation were calculated: a of Hill's equation (relating to the isometric peak tension) = 0.36; b (relating to the actual muscle length) = 0.19 ML/s; VM Trelating to the actual muscle length) = 0.56 ML/s. Within the range of pCa between 2.0 and 3.2 the amount of force generation (= delta P) depended on the extracellular calcium level whereas the extrapolated velocity of shortening of the unloaded preparation (= VM) did not. Also pH changes between 8.0 and 6.8 as well as noradrenaline incubation at a pH of 5.9 affected delta P quite considerably, but VM only scarcely. At a pH of 6.3, however, VM was distinctly diminished, and a reduced calcium sensitivity of the ATPase was inferred from the shift of ED50 of extracellular calcium from 0.66 mM Ca at a pH of 7.3 to 1.56 mM Ca at a pH of 6.3 (P less than 0.0005). It is concluded from these results that the experimental conditions-pCa between 2.0 and 3.2, pH between 8.0 and 6.8, and noradrenaline added at a pH of 5.9-obviously change the intracellular calcium concentration which influences the number of activated interaction sites rather than the velocity of crossbridge movement.
Explore the source record for details and available documents.
Force velocity relationships of isolated vascular smooth muscle preparations were examined in the tetanized rat portal--anterior mesenteric vein by means of afterloaded isotonic contractions. Lowering of the temperature from 37 degrees C to 25 degrees C caused an average decrease of the follwoing parameters: maximal velocity of shortening at zero load from 0.51 to 0.28 muscle length/sec; maximal rate of tension increase (dT/dt) from 847 to 362 dyn/sec; mechanical tension developed at the maximum of dT/dt from 43 to 34% of the peak force generation; constant b of Hill's equation from 0.18 to 0.09 muscle length/sec. The latency was prolonged from 0.33 to 0.56 sec, and the time-to-maximum of dT/dt from 0.9 to 1.6 sec. Between 27 degrees C and 37 degrees C the following Q10 values were calculated: for the maximal velocity of shortening at zero load 1.56; for the maximal rate of tension increase 1.88; for the latency 1.63. No distinct influence of temperature could be observed on the extent of isotonic shortening at zero load (3.69 muscle length at 37 degrees C), on the extent of peak force generation (1107 dyn at 37 degrees C), and on constant a of Hill's equation (0.35 at 37 degrees C). It is concluded that parameters of contraction velocity in vascular smooth muscle depend on temperature, whereas the extent of contraction is independent of temperature. These findings are discussed in connection with the theory of the sliding-filament mechanism.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Stretching of K-depolarized contracted helically cut strips of pig coronary arteries produced a delayed increase in tension. The influence of temperature and extracellular calcium on this active response to stretch was investigated. Reference for all tension values was the amplitude of contraction (induced by K-depolarization) starting from the high resting tension. 1. The mean amplitude of the delayed tension increase after stretch amounted to 27.5 plus or minus 4.8% (x plus or minus SEM, n equals 9); lowering the bath temperature from 37 degrees C to 27 degrees C caused a drop to 10.8 plus or minus 1.5% (n equals 9; P smaller than 0.0025); increasing the calcium concentration of the bath solution from 2.7 to 6.9 mM produced negligible effects on both the amplitude of the delayed tension increase (24.6 plus or minus 1.0%; n equals 9), and the amplitude of contraction after depolarization. 2. The peak tension time of the active response to stretch was not changed by the 6.9 mM calcium, but prolonged from 27.9 plus or minus 4.0 to 40.7 plus or minus 4.4 minutes (P smaller than 0.025) by lowering the bath temperature to 27 degrees C. At the high calcium level the preparation contracted faster after depolarization than at the normal calcium level. 3. The experimental results correspond with the conception of the sliding filament mechanism as the basic process of contraction also in vascular smooth muscle preparations. The delayed tension increase after stretch may be caused by a recruitment of interaction sites between contractile proteins.
Explore the source record for details and available documents.
The effect of adrenergic stimulating and inhibiting drugson the prostaglandin-dependent colonmotility in man was examined. By stimulating the adrenergic beta-receptors the prostaglandin-induced contractions were reduced and finally eliminated...