The effect of adrenaline on the tension developed in contractures and twitches of the ventricle of the frog.
1. The effect of adrenaline on contracture and twitch tension in frog's ventricle has been examined, using the superfused preparation.2. In 1 mM-Ca Ringer, contractures induced with excess KCl concentrations from 50 to 200 mM, are reduced by 1 x 10(-6) g/ml. adrenaline to an average of 0.62 of control values, in marked contrast to the well known positive inotropic effect of adrenaline on the heart twitch. This effect of adrenaline is directly dose dependent. Increasing [Ca](o) diminishes the effect of adrenaline on contracture tension, and on the twitch tension.3. Adrenaline has a significantly greater effect on the KCl contracture tension than noradrenaline or isoprenaline.4. In 1 mM-Ca Ringer, Na-free contractures are reduced to 0.72 of controls by 1 x 10(-6) g/ml. adrenaline. Adrenaline also significantly reduces tension in contractures induced by 50 c/s alternating current.5. The action of adrenaline on contracture tension is largely complete in 1-2 min at various rates of stimulation and calcium concentrations. A similar time course has been found for the effect of adrenaline on membrane potential.6. Pronethalol blocks the action of adrenaline on both twitch and contracture. The action on the contracture can also be blocked by ouabain (1 x 10(-5)M), and exposure of the tissue to K-free or Na-free Ringer solution.7. Adrenaline hyperpolarizes the membrane potential with a range of [K](o) from 0 to 200 mM. This effect is blocked by pronethalol and ouabain. After exposure to ouabain, adrenaline causes a significant decrease in the membrane potential. This may be due to an increase in the sodium permeability.8. At low values of the [Ca]/[Na](2) ratio, adrenaline takes a relatively constant number of beats for full action, but at high values of the ratio the development of full effect is largely time dependent.9. The time course of the effect on the twitch of changing from 0.5 to 2 mM-Ca Ringer has been studied at various rates of stimulation. The equilibration time has been found to depend on the heart rate.10. The effect on the contracture suggests that adrenaline decreases the calcium permeability. It is further suggested that the development of twitch tension is not due to direct Ca entry but is due to the release of Ca from a local store within or between the cells. The inotropic action of adrenaline is explained in terms of this store.
D000818:Animals; D001001:Anura; D001696:Biomechanical Phenomena; D002118:Calcium / Q000494:pharmacology; D002463:Cell Membrane Permeability; D004558:Electric Stimulation; D004837:Epinephrine / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects*; D006352:Heart Ventricles / Q000187:drug effects; D066298:In Vitro Techniques; D007545:Isoproterenol / Q000494:pharmacology; D007552:Isotonic Solutions; D008564:Membrane Potentials / Q000187:drug effects; D009119:Muscle Contraction / Q000187:drug effects*; D009638:Norepinephrine / Q000494:pharmacology; D011189:Potassium Chloride / Q000494:pharmacology; D012964:Sodium / Q000378:metabolism; D013997:Time Factors
D007552:Isotonic Solutions; D011189:Potassium Chloride; D012964:Sodium; D007545:Isoproterenol; D002118:Calcium; D009638:Norepinephrine; D004837:Epinephrine