Preganglionic stimulation of the cat's superior cervical ganglion at 60/s for 2–8 min reduced the ganglion's acetylcholine (ACh) content by about 30%. With continued stimulation, the ACh stores gradually recovered within 15 min. However, when ganglia were allowed to rest following 4 min of stimulation at 60/s not only was there a rapid restoration of the ACh content, but the ACh levels rose to 130% of control after 10 min of rest. Under either of these experimental conditions the choline content increased transiently only after the ACh stores had returned to control values. The above data suggest that there may be a delay in the onset of maximal rates of ACh resynthesis induced by nerve stimulation and that ACh synthesis continues for several minutes after the cessation of the stimulus. In addition, the results are consistent with the concept that about one-third or more of the total ACh stores of a rested ganglion is in a form that can be readily mobilized for release. The observed rebound increase in the ACh content probably means that the ACh storage capacity is not normally saturable and that under most physiological conditions the ACh levels are maintained within certain limits by a precise control of ACh synthesis.

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An investigation of changes in the Mg2+ -dependent, Na+ -K+ -stimulated sarcolemmal ATPase and of intracellular electrolytes in the left failing heart due to pressure overload (aortic banding) was carried out in dogs. There was no change in the sarcolemmal Mg2+ -ATPase of the left or right ventricle for the whole duration (3 to 9 months) of left ventricular pressure overload. In the early phase (3 months) of aortic banding, when there was no haemodynamic evidence of left ventricular failure, there was also no significant change in the sarcolemmal Na+ -K+ -ATPase, extracellular space, or intra- and extracellular electrolytes. However, during 6 to 9 months of aortic binding when there was haemodynamic evidence of left ventricular failure (increased end-diastolic pressure, decreased cardiac index and (dP/dt)/IIP, enlarged heart), there was also a marked increase in the left ventricular sarcolemmal Na+ -K+ -ATPase and intracellular K+; and a decrease in the intracellular Na+ and Ca2+. The extracellular space in the left ventricle also increased significantly. Unlike the left ventricle, the right ventricle did not show any evidence of failure, not did it show any change in the sarcolemmal Na+ -K+ -ATPase and intracellular electrolytes during any period of aortic banding. These results suggest that the decrease in the myocardial contractility in failing heart due to pressure overload might be associated with a decrease in the intracellular Ca2+ as a result of an increase in the sarcolemmal Na+ -K+ -ATPase.