The effects of acetylcholine and catecholamines on post-rest phenomena in rabbit and guinea-pig atria and on accompanying shifts of 45Ca in guinea-pig atrial muscle

Abstract

We studied the pattern of post-rest activation and shifts of 45Ca in the isolated mammalian atrial muscle. The first contraction evoked in the rabbit and guinea-pig atrial muscle after 10 min rest was several times stronger than the steady-state beats at a rate of 60/min. Contractile force (CF) declined to 20-50% of control during the next 1-3 beats and recovered to the pre-rest level upon subsequent stimulation. The post-rest beats were negligibly affected by noradrenaline (NA), isoproterenol (IS) acetylcholine (ACh), carbachol (CCh) and Ni, whereas the steady-state beats were readily affected by all these drugs or ions. Post-rest potentiation was completely inhibited by caffeine in a concentration of 10 mM. The guinea-pig atria, equilibrated for 60 min in 45Ca containing solution and stimulated at a rate of 60/min, contained 4.47 +/- 0.16 mmol 45Ca/kg wet weight (w.w.). Ten min of rest resulted in a drop of this content to 3.52 +/- 0.13 mmol/kg w.w. despite the continued presence of 45Ca in the superfusing solution. Three initial post-rest beats resulted in further drop of the content of 45Ca to 2.62 +/- 0.14 mmol/kg w.w. Continued post-rest stimulation resulted in a recovery of the pre-rest 45Ca content. This recovery was inhibited by ACh and CCh. Both drugs inhibited 45Ca loss during the initial 3 beats. Neither this loss nor recovery were affected by IS. It is concluded that calcium (Ca) fraction described in the previous papers [11, 15] as Ca2 in the guinea-pig ventricular muscle plays an important role in the force-frequency relations also in the atrial muscle. However, unlike in ventricular muscle only about half of it is released from the cells upon rest whereas the remaining Ca is taken up by the release compartment and used to activate the strong post-rest contraction. It is thereafter extruded from the cells which results in severe depletion of intracellular Ca stores. Fraction Ca2 is re-accumulated during the post-rest stimulation resulting in recovery of the contractile force.