TY - JOUR
T1 - Effects of alpha(1)- or beta-adrenoceptor stimulation on work-loop and isometric contractions of isolated rat cardiac trabeculae
AU - Layland, J
AU - Kentish, J C
PY - 2000
Y1 - 2000
N2 - 1. We studied the effects of alpha(1)- or beta-adrenoceptor stimulation on the contractility of isolated rat ventricular trabeculae at 24 degrees C using the work-loop technique, which simulates the cyclical changes in length and force that occur during the cardiac cycle. Some muscles were injected with fura-2 to monitor the intracellular Ca2+ transient. 2. Comparison of twitch records revealed that peak force was greater and was reached earlier in work-loop contractions than in corresponding isometric contractions. This was attributed to the changes in muscle length and velocity during work-loop contractions, since the Ca2+ transients were largely unaffected by the length changes. 3. Stimulation of alpha(1)-adrenoceptors (with 100 mu M phenylephrine) increased net work, power production, the frequency for maximum work, and the frequency for maximum power production (f(opt)). The increase in net work was due to the positive inotropic effect of phenylephrine, which was similar at all frequencies investigated (0.33-4.5 Hz). The increase in f(opt) was attributed to an abbreviation of twitch duration induced by alpha(1)-stimulation at higher frequencies(> 1 Hz), even though the twitch became longer at 0.33 Hz. 4. beta-Adrenoceptor stimulation (with 5 mu M isoprenaline) produced marked increases in net work, power output, the frequency for net work, and f(opt). These effects were attributed both to the positive inotropic effect of beta-stimulation, which was greater at higher frequencies, and to the reduction in twitch duration. beta-Stimulation also abolished the frequency-dependent acceleration of twitch duration. 5. The increase in power output and f(opt) with alpha(1)- as well as beta-adrenoceptor stimulation suggested that both receptor types may contribute to the effects of catecholamines, released during stress or exercise, although the greater effects of beta-stimulation are likely to predominate.
AB - 1. We studied the effects of alpha(1)- or beta-adrenoceptor stimulation on the contractility of isolated rat ventricular trabeculae at 24 degrees C using the work-loop technique, which simulates the cyclical changes in length and force that occur during the cardiac cycle. Some muscles were injected with fura-2 to monitor the intracellular Ca2+ transient. 2. Comparison of twitch records revealed that peak force was greater and was reached earlier in work-loop contractions than in corresponding isometric contractions. This was attributed to the changes in muscle length and velocity during work-loop contractions, since the Ca2+ transients were largely unaffected by the length changes. 3. Stimulation of alpha(1)-adrenoceptors (with 100 mu M phenylephrine) increased net work, power production, the frequency for maximum work, and the frequency for maximum power production (f(opt)). The increase in net work was due to the positive inotropic effect of phenylephrine, which was similar at all frequencies investigated (0.33-4.5 Hz). The increase in f(opt) was attributed to an abbreviation of twitch duration induced by alpha(1)-stimulation at higher frequencies(> 1 Hz), even though the twitch became longer at 0.33 Hz. 4. beta-Adrenoceptor stimulation (with 5 mu M isoprenaline) produced marked increases in net work, power output, the frequency for net work, and f(opt). These effects were attributed both to the positive inotropic effect of beta-stimulation, which was greater at higher frequencies, and to the reduction in twitch duration. beta-Stimulation also abolished the frequency-dependent acceleration of twitch duration. 5. The increase in power output and f(opt) with alpha(1)- as well as beta-adrenoceptor stimulation suggested that both receptor types may contribute to the effects of catecholamines, released during stress or exercise, although the greater effects of beta-stimulation are likely to predominate.
U2 - 10.1111/j.1469-7793.2000.t01-1-00205.x
DO - 10.1111/j.1469-7793.2000.t01-1-00205.x
M3 - Article
SN - 1469-7793
VL - 524
SP - 205
EP - 219
JO - The Journal of Physiology
JF - The Journal of Physiology
IS - 1
ER -